{"id":22844,"date":"2026-06-19T10:30:56","date_gmt":"2026-06-19T08:30:56","guid":{"rendered":"https:\/\/www.biolife-publisher.it\/ejnd\/?p=22844"},"modified":"2026-06-19T10:30:56","modified_gmt":"2026-06-19T08:30:56","slug":"the-far-reaching-consequences-of-covid-19-on-inflammatory-diseases-a-narrative-review","status":"publish","type":"post","link":"https:\/\/www.biolife-publisher.it\/ejnd\/2026\/06\/19\/the-far-reaching-consequences-of-covid-19-on-inflammatory-diseases-a-narrative-review\/","title":{"rendered":"THE FAR-REACHING CONSEQUENCES OF COVID-19 ON INFLAMMATORY DISEASES: A NARRATIVE REVIEW"},"content":{"rendered":"

C. Genovesi1*<\/sup> and R. Grilli2<\/sup><\/p>\n

1 <\/sup>Skin Centres, Private Practice, Avezzano-Pescara, Italy;
\n2 <\/sup>Dentistry, Private Practice, Chieti-Pescara, Italy.<\/p>\n

*Correspondence to<\/em>:
\nCorinna Genovesi,
\nSkin Centres,
\nPrivate Practice,
\nAvezzano-Pescara, Italy.
\ne-mail: corinnagenovesi@gmail.com<\/p>\n\n\n\n
Received: 20 March, 2026
\nAccepted: 19 June, 2026
\n\"adobe-pdf-download-icon\"<\/a><\/td>\n		ISSN 2279-5855 print \/ 3103-7364 [online]
\nCopyright 2026 \u00a9 by Biolife Publisher
\nThis publication and\/or article is for individual use only and may not be further reproduced without written permission from the copyright holder. Unauthorized reproduction may result in financial and other penalties. Disclosure: All authors report no conflicts of interest relevant to this article.<\/td>\n<\/tr>\n<\/tbody>\n<\/table>\n

ABSTRACT<\/strong><\/p>\n

This narrative review aims to provide an overview of the effects of Coronavirus disease 2019 (COVID-19) infection on pre-existing systemic inflammatory conditions, including type 2 diabetes mellitus, cardiovascular diseases, multiple sclerosis, systemic lupus erythematosus, gastrointestinal diseases, and local conditions with significant systemic repercussions such as periodontal disease. By studying the mechanisms triggered by the virus, it can be hypothesised that severe acute respiratory syndrome coronavirus 2 (SARS\u2011CoV\u20112) may be the cause of the worsening of these conditions following recovery. In particular, persistent inflammation, the cytokine storm, antibodies and endothelial damage, combined with the psychological stress caused by the pandemic, are the factors that could explain the worsening of systemic conditions.<\/p>\n

KEYWORDS<\/strong>: SARS-CoV-2, cytokine storm, long Covid, systemic inflammation, autoimmunity<\/p>\n

\u00a0<\/strong><\/p>\n

INTRODUCTION<\/strong><\/p>\n

 <\/p>\n

Coronavirus disease 2019 (COVID-19) is an acute respiratory illness caused by severe acute respiratory syndrome coronavirus 2 (SARS\u2011CoV\u20112), a virus belonging to the coronavirus family. The COVID-19 pandemic was declared by the World Health Organization in March 2020 and has had a significant impact on the health of the global population, with important consequences for the future as well. SARS-CoV-2 caused respiratory infections manifesting with symptoms such as cough, fever, headache and gastrointestinal irritation. Conversely, in some cases (namely in asymptomatic patients) these symptoms did not occur. The importance of detecting the infection was linked to the risk of severe pneumonia and potential patient mortality, particularly in elderly individuals or those already suffering from immunological disorders (1).<\/p>\n

Numerous articles have highlighted that the main receptor to which the virus binds in order to penetrate cells is the angiotensin-converting enzyme 2 (ACE2) receptor, a receptor present in all major metabolic tissues and organs, including the lungs, kidneys, adipose tissue and pancreatic \u03b2-cells, which is why the symptoms of the infection can affect various systems and organs of the body (2).<\/p>\n

It is evident from the literature that particular attention must be paid especially to patients with comorbidities such as diabetes, hypertension and cardiovascular disease, who are at greater risk of experiencing significant post-COVID-19 complications (3).<\/p>\n

This narrative review addresses the significant consequences of COVID-19 on major systemic inflammatory diseases, highlighting the factors triggered by the infection that may contribute to the worsening of these conditions. Some of these factors include the cytokine storm, epithelial damage and the onset of autoantibodies, mechanisms that overlap with the systemic consequences of pandemic-induced psychological stress.<\/p>\n

 <\/p>\n

MATERIALS AND METHODS<\/strong><\/p>\n

 <\/p>\n

This review includes studies that have examined the consequences of the pandemic on the systemic and psychological health of the population and have hypothesised the possible causes of the worsening of certain inflammatory diseases. The sources of the publications analysed are the PubMed and Embase databases from 2022 to the present.<\/p>\n

 <\/p>\n

RESULTS<\/strong><\/p>\n

 <\/p>\n

Inflammatory diseases and COVID-19 <\/em><\/p>\n

Although the effects of the initial phase of the disease are well known, there is less evidence in the literature regarding the long-term consequences of COVID-19 infection (4).<\/p>\n

Some researchers have found that individuals infected with this virus not only exhibited acute inflammation during the clinical phase but also developed a persistent pro-inflammatory gene signature over time. The presence of this transcriptional marker indicates that, even months after infection, certain immune cells continue to express genes associated with inflammatory processes (5).<\/p>\n

Furthermore, the same study highlights that COVID-19 can trigger or amplify chronic inflammatory mechanisms, exhibiting a gene expression pattern like that observed in autoimmune and chronic inflammatory diseases. SARS-CoV-2 infection, therefore, does not disappear completely when the swab test returns negative, as it can leave a lasting pro-inflammatory molecular imprint potentially involved in the worsening or onset of chronic inflammatory diseases (6).<\/p>\n

Further articles in the literature support the correlation between COVID-19 and the worsening of systemic inflammatory diseases and confirm that the infection in question may contribute to the reactivation, worsening and persistence of inflammation in patients with autoimmune and anti-inflammatory conditions. This occurs because COVID-19 infection, by overlapping with pre-existing inflammatory mechanisms, amplifies the production of inflammatory cytokines and alters the systemic immune balance (7).<\/p>\n

The cited article discusses the immunological pathways shared by COVID-19 infection and systemic diseases: those involving interleukin-6 (IL-6), tumor necrosis factor alpha (TNF-\u03b1) and interferons (INFs). IL-6, a key pro-inflammatory cytokine in inflammatory joint diseases, is also involved in the systemic inflammatory response observed in COVID-19. TNF-\u03b1, a mediator of chronic inflammation, and INFs, which play an essential role in the early antiviral response, are both altered in patients with COVID-19, highlighting the possibility that the virus may amplify pre-existing inflammatory mechanisms (8).<\/p>\n

\u00a0<\/em><\/p>\n

Correlation with type 2 diabetes mellitus<\/em><\/p>\n

Type 2 diabetes is a chronic metabolic disease characterised by hyperglycaemia and caused by high insulin resistance in tissues or reduced insulin production. The condition can cause significant systemic complications, including kidney damage and cardiovascular disease, and the co-occurrence of hyperglycaemia with other risk factors such as heart disease could be fatal for the patient. It is therefore essential to monitor diabetic patients, as coronavirus infection, in this case, has an even greater impact (9).<\/p>\n

The potential pathogenic correlation between diabetes mellitus and COVID-19 involves glucose homeostasis, inflammation, an altered immune status, and activation of the renin-angiotensin-aldosterone system (RAAS), a hormonal mechanism that regulates blood pressure, circulating plasma volume, and arterial muscle tone. In particular, the RAAS involves an enzyme responsible for converting angiotensin I into angiotensin II, namely angiotensin-converting enzyme 2 (ACE2), and in diabetic patients, excessive production of angiotensin II occurs due to chronic activation of the RAAS. Excess angiotensin II causes vasoconstriction of the afferent arteriole and an increase in intraglomerular pressure, leading to renal damage over time.<\/p>\n

SARS-CoV-2 exploits the ACE2 present in the pulmonary capillaries to enter cells, as the enzyme is the primary receptor for this virus (10).<\/p>\n

As previously stated, the virus enters cells by binding primarily to the ACE2 receptor and, consequently, in the event of infection, the normal glucose metabolism pathway may be compromised, increasing the risk of hyperglycaemia and other pathological mechanisms. The receptor in question is also expressed in pancreatic tissues, allowing the virus free access to penetrate \u03b2-cells and impairing their endocrine function of producing insulin (11). A severe infection also alters the immune response which, combined with hyperglycaemia, significantly worsens inflammation.<\/p>\n

Furthermore, SARS-CoV-2 exacerbates pre-existing endothelial damage in diabetic patients, promoting hypercoagulation and, consequently, increasing the risk of thrombosis.<\/p>\n

Furthermore, glucocorticoid-based therapies, medicines commonly used in the treatment of severe cases of COVID-19, may promote the progression of hyperglycaemia and insulin resistance. This negative influence on glucose metabolism is due to increased glucose production by the liver and reduced peripheral glucose utilisation, which raises blood sugar levels. For this reason, glucocorticoid therapy for COVID-19 should be avoided in patients with diabetes so as not to exacerbate existing hyperglycaemia (12).<\/p>\n

In summary, the virus\u2019s impact on \u03b2-cells through direct invasion or systemic inflammation can induce insulin resistance and compromise glucose homeostasis (13).<\/p>\n

As also confirmed by longitudinal studies, COVID-19 can act as an amplifier of pre-existing systemic conditions such as type 2 diabetes mellitus, as the infection can increase insulin resistance and damage \u03b2-cells, compromising metabolic stability even months after recovery from the infection.<\/p>\n

 <\/p>\n

Correlation with periodontal disease <\/em><\/p>\n

The link between systemic diseases and periodontitis is already well established in the literature. Periodontitis involves inflammation of the tissues supporting the teeth and can significantly affect a patient\u2019s systemic health (14).<\/p>\n

Furthermore, periodontal disease can worsen in the presence of respiratory conditions, including COVID-19, because both diseases share the same inflammatory mediators and, consequently, their relationship is bidirectional. The worsening of systemic diseases following COVID-19 infection may be due to persistent systemic inflammation, as many patients maintain high levels of IL-6 and other markers for weeks, to endothelial damage caused by the virus, and to immune dysfunction such as lymphopenia and neutrophil dysfunction.<\/p>\n

In addition, it has been shown that psychological stress may also be involved in the worsening of periodontitis. This factor, in fact, increases cortisol levels, reduces immune defences and increases pro-inflammatory cytokines. Consequently, psychological stress, anxiety and depression induced by the pandemic and the disease itself may worsen periodontal disease (15-17).<\/p>\n

 <\/p>\n

Correlation with rheumatoid arthritis <\/em><\/p>\n

Rheumatoid arthritis (RA) is a chronic autoimmune inflammatory disease that affects the small joints of the hands and feet, as well as other areas. It is unclear whether patients with RA or those taking certain disease-modifying antirheumatic drugs (DMARDs) are at greater risk of experiencing significant post-COVID-19 complications; however, conversely, individuals with RA undergoing glucocorticoid therapy appear to be at greater risk. Taking prednisone, for example, at a dose exceeding 10 mg per day, may increase the risk of hospitalisation and lead to worse clinical outcomes from COVID-19 (18).<\/p>\n

Furthermore, the pandemic has posed significant challenges for RA patients in terms of access to care, drug shortages, social isolation and anxiety, factors that may be associated with disease flare-ups. Here too, psychological health plays a fundamental role, and the article by Kristin M. D\u2019Silva and Zachary S. Wallace highlights how psychological stress resulting from limited access to care, drug shortages and complete isolation has led to unpleasant long-term repercussions for patients with RA (19).<\/p>\n

\u00a0<\/em><\/p>\n

Correlation with multiple sclerosis <\/em><\/p>\n

Multiple sclerosis (MS) is a chronic neurodegenerative disease affecting the central nervous system. Specifically, MS is an autoimmune and demyelinating disease, meaning it causes a progressive loss of the myelin sheaths that surround and insulate nerve fibres (20).<\/p>\n

The study by Nahad Sedaghat et al. compared the pre-COVID and post-COVID periods in patients with relapsing-remitting multiple sclerosis (RRMS), the most common form of MS. The study aims to gather evidence on the increase in relapses and the overall clinical activity of the disease in the post-infection phase. Relapses refer to the onset or worsening of neurological symptoms such as localised weakness, balance difficulties or visual disturbances, whilst overall clinical activity encompasses the number of relapses, the persistence of symptoms over time and the worsening of disability.<\/p>\n

Furthermore, the virus may influence the course of the disease because it can disrupt the immunological balance of RRMS, a dynamic equilibrium between autoimmune attack and immune control. This balance can be disrupted by immunological stress or infections, including COVID-19 infection, and, as a result, the inflammatory mechanisms responsible for relapses are not counterbalanced by the regulatory mechanisms that normally maintain remission.<\/p>\n

Although no direct correlation with multiple sclerosis emerges from the study, the virus is recognised as a factor that can increase clinical activity in RRSM and, for this reason, the authors highlight the need for clinical monitoring following infection (21).<\/p>\n

 <\/p>\n

Correlation with systemic lupus erythematosus <\/em><\/p>\n

Systemic lupus erythematosus (SLE) is a chronic autoimmune inflammatory condition that can affect any organ or system in the body. The condition shares significant similarities with COVID-19, including the activation and dysfunction of endothelial cells and the activation of the complement system, the presence of antiphospholipid antibodies, and the formation of Neutrophil Extracellular Traps (NETs). In both conditions, autoimmunity promotes hyperinflammatory, hypercoagulable and hypofibrinolytic states and their thromboembolic complications, including the development of atherosclerotic plaques and myocardial ischaemia (22).<\/p>\n

Numerous studies have been conducted to investigate how the pandemic has affected patients with SLE, and it has emerged that, as also highlighted in other systemic diseases, psychological stress can play an important role in the worsening of the disease. The literature has already extensively documented that patients with autoimmune diseases such as SLE are more vulnerable to psychological stressors and are at high risk of anxiety and depression in the event of COVID-19 infection (23).<\/p>\n

Firstly, it is possible to investigate a correlation between SLE and COVID-19 as a similarity in the immunopathogenic characteristics of the two conditions has already been documented: the expression of type I INF and the cytokine storm.<\/p>\n

As previously stated, COVID-19 infection begins with the virus binding to the human angiotensin-converting enzyme 2 (hACE2) receptor, thereby entering the epithelial cells of the pulmonary alveoli and triggering a strong immuno-inflammatory response. Subsequently, the onset of autoantibodies can be risky, particularly in genetically predisposed individuals, and may promote the development of autoimmune diseases.<\/p>\n

COVID-19 and SLE share the same immunological characteristics, including the action of type 1 INF, which is generally elevated in patients with SLE. Although INF protects the body from a hyperinflammatory response to COVID and activates plasmacytoid dendritic cells (pDCs) that help combat the virus, excessive INF activity can cause a skin rash with small-vessel thrombosis and an inflammatory infiltrate similar to lupus erythematosus. Furthermore, the cytokine storm plays a key role in both conditions as it recruits neutrophils and macrophages, produces large quantities of cytokines and activates CD4 and CD8 lymphocytes (24).<\/p>\n

Furthermore, SARS-CoV-2 infection can induce antiphospholipid antibodies, which may be among the factors responsible for the increased risk of thrombosis observed in patients infected with the virus. This occurs because these autoantibodies make the blood more prone to clotting, and in SLE patients who already chronically produce antiphospholipid antibodies, the infection may promote hypercoagulability, thereby increasing the risk of thrombosis.<\/p>\n

Additionally, the risk of thrombosis may be exacerbated by the endothelial dysfunction that occurs in both conditions: in SLE patients, chronic inflammation promotes the accumulation of cells and fats in the endothelial wall, and this damage, in the event of SARS-CoV-2- l infection, is not only amplified but may also persist for months, providing a fertile ground for the formation of atherosclerotic plaques and clots (25).<\/p>\n

The study conducted by Yi You et al. highlights that post-COVID-19 complications, including thrombosis and respiratory failure, may result from complement hyperactivation, which is responsible for the recruitment of leukocytes that trigger the cytokine storm. The release of pro-inflammatory cytokines, including IL-1, IL-6, IL-8, and INF-\u03b3, can cause microvascular damage (26).<\/p>\n

Furthermore, the study by Timsit et al. confirms that severe COVID-19 infections are followed by the emergence of autoantibodies that cause alterations in tolerance mechanisms due to rapid and exaggerated inflammatory responses to SARS-CoV-2. In particular, critically ill patients with COVID-19 show intense extrafollicular B-cell responses enriched with potential autoreactivity, similar to what occurs in patients with SLE. Extrafollicular expansion may be responsible for flares in patients with SLE (27).<\/p>\n

Another clinical study compares the number of flares detected in SLE patients with and without COVID-19 within 90 days of infection, confirming that the risk of flare-ups may increase significantly in the event of SARS-CoV-2 infection. In support of the previously cited article, the researchers highlighted that in patients with systemic lupus erythematosus, self-tolerance is lost with the activation of B and T cells and, consequently, autoantibodies are produced that mediate tissue damage.<\/p>\n

Furthermore, based on the data collected, the authors hypothesise that the worsening of SLE may be associated with peak cytokine release, TLR activation, and the INF and Nuclear Factor kappa-light-chain-enhancer of activated B cells (NF-\u03baB) responses, factors that create a pro-inflammatory environment. The autoimmune response may be amplified by autoreactive B and T cells stimulated by the virus. Even in the absence of severe flares, immune mechanisms linked to inflammation can break down immunological tolerance and reactivate the chronic disease, worsening the condition (28).<\/p>\n

Finally, according to the cited studies, COVID-19 infection may act as an aggravating factor in autoimmune disease by contributing to the amplification of inflammation and increasing the risk of endothelial damage and thrombosis.<\/p>\n

 <\/p>\n

Correlation with cardiovascular diseases <\/em><\/p>\n

Cardiovascular diseases are strongly correlated with periodontal disease and, for this reason, may worsen in the post-COVID phase for the same reasons: the persistence of inflammation, endothelial dysfunction, microthrombosis and an altered immune response (29).<\/p>\n

These virus-induced factors can perpetuate cardiovascular damage over time, even after the swab test returns a negative result.<\/p>\n

The study by Stefan Neubauer et al. highlights that cardiac abnormalities, including fibrosis and myocardial oedema, have been detected in many patients even in the absence of persistent cardiovascular disease. Based on advanced tests conducted in these patients, it is evident that COVID-19 infection can worsen cardiovascular disease even in a \u2018silent\u2019 manner that is not immediately clinically detectable.<\/p>\n

Finally, among the potential consequences of the virus in patients with cardiovascular disease are worsening cardiac dysfunction and an increased risk of heart failure. Consequently, COVID-19 can act as an amplifier of an already existing vulnerability (30).<\/p>\n

In cases of cardiac damage, an increase in biomarkers, including troponin and N-terminal pro B-type natriuretic peptide (NT-proBNP), has been observed; furthermore, echocardiographic assessment carried out months after recovery reveals structural and functional changes in the heart. Among the documented cardiovascular complications, the most common are deep vein thrombosis (DVT), increased thromboembolic risk and prolonged cardiac dysfunction.<\/p>\n

It is clear that the function of the heart and blood vessels, which was already compromised prior to infection, is severely strained by the chronic inflammation triggered by the infection and the resulting disruption of the immune response.\u00a0 The study therefore supports the theory that long COVID may contribute to and exacerbate the progression of pre-existing cardiovascular conditions (31-32).<\/p>\n

 <\/p>\n

Correlation with gastrointestinal diseases <\/em><\/p>\n

Gastrointestinal diseases refer to all disorders affecting the stomach and small intestine, including gastritis and gastroduodenitis, which, according to the scientific literature, share similar inflammatory processes; the common targets for both diseases could be the ACE2 and IL-17 pathways (33).<\/p>\n

As previously stated, the ACE2 receptor is also expressed in the intestine, and SARS-CoV-2 can enter human cells by recognizing this receptor. The main functions of ACE2 are to regulate the renin-angiotensin system, contribute to local anti-inflammatory processes, and maintain the intestinal barrier. If the virus binds to ACE2, the inflammatory balance is disrupted, protective function is reduced, and the risk of dysbiosis and increased intestinal permeability rises, factors that can cause severe damage to the intestinal mucosa and compromise the intestine\u2019s digestive and absorptive function, potentially contributing to the worsening of GI symptoms.<\/p>\n

Furthermore, interleukin-17 is also involved in the pathogenesis of IBD and plays key roles, including the recruitment of neutrophils and the amplification of the inflammatory response. In the case of COVID-19 infection, IL-17 activates Th17 cells and increases IL-6, stimulating mucosal inflammation, which is why the infection could exacerbate gastrointestinal pathology (34).<\/p>\n

Finally, the same study demonstrated that epithelial cells of the intestinal tract are highly susceptible to the virus and promote its replication; therefore, patients infected with the virus may be at a higher risk of developing gastrointestinal diseases. By comparing the severity of COVID-19 infection between patients with and without GI symptoms, it was found that patients with GI symptoms had a significantly more severe infection, and this correlation may support the hypothesis that intestinal manifestations of COVID-19 can further exacerbate pre-existing gastrointestinal diseases. Despite numerous studies on the potential association between the two conditions, further research is needed to confirm that this correlation is not coincidental (35).<\/p>\n

Furthermore, the virus in question enters cells via the ACE2 receptor, which is present in many types of cells, including those of the lungs, the oral cavity, the nose, and also the gastrointestinal tract mucosa; this is why COVID-19 symptoms may include bloating, diarrhoea, abdominal discomfort, nausea and vomiting. A study conducted in 2020 by Drossman et al. recorded the prevalence and severity of these manifestations in approximately 2,000 patients with COVID-19 and assessed the persistence of these symptoms and the potential development of gut-brain interaction disorders (GBID) more than 12 months later.<\/p>\n

The recorded data show that 42% of patients who presented with COVID-related gastrointestinal symptoms during hospitalisation retained at least one of these symptoms at follow-up; furthermore, the severity of these persistent symptoms increased in those who developed gut-brain interaction (GBI). These same patients also presented with a stress disorder associated with hospitalisation for COVID; therefore, the study not only confirms the association between the virus and prolonged gastrointestinal symptoms but also highlights the need for interventions aimed at reducing post-traumatic stress to, in turn, mitigate prolonged gastrointestinal symptoms (36).<\/p>\n

Finally, a genomic molecular study was conducted which, in addition to confirming that COVID-19 infection can stimulate intense inflammatory responses similar to those observed in patients with GBID disorders, hypothesises that the cytokine storm induced by the virus may amplify intestinal inflammation, thereby worsening the condition. The cited study initially analysed databases of patients with GI disorders, patients with COVID-19 and healthy controls to investigate the presence of abnormally expressed genes in both conditions, common inflammatory pathways and possible shared molecular mechanisms.<\/p>\n

As has emerged in relation to other systemic conditions, SARS-CoV-2 infection and gastrointestinal disorders (GI) share a similar immune inflammatory signature. This similarity has been demonstrated by the identification of differentially expressed genes (DEGs), genes common to both COVID and inflammatory bowel disease (IBD). In the inflammatory response, the key role is played by interleukin 6, which is elevated in both severe COVID and IBD flares. IL-6 stimulates the liver\u2019s production of acute-phase proteins such as C-reactive protein; consequently, in the event of a rise in systemic IL-6 due to SARS-CoV-2 infection and in the presence of pre-existing gastrointestinal symptoms, IBD can exacerbate mucosal inflammation. Another interleukin involved is IL-1\u03b2 (Interleukin-1 beta), which contributes to tissue damage. TNF-\u03b1 also plays a central role in the pathogenesis of IBD and is heavily involved in the cytokine storm typical of COVID-19 infection. Among the INFs involved, IFN-\u03b3 is one of the main ones and is responsible for the activation of macrophages and enhances the Th1 response.<\/p>\n

The intercellular pathways involved are the Janus Kinase \/ Signal Transducer and Activator of Transcription (JAK\/STAT) pathway, which transmits the cytokine signal to the nucleus and activates inflammatory genes, and the NF-\u03baB pathway, which primarily regulates inflammation and triggers the transcription of IL-6, TNF, IL-1\u03b2, etc.<\/p>\n

The mechanism hypothesised by the study to explain the worsening of GI disorders is as follows: SARS-CoV-2 enters intestinal cells via the ACE2 receptor, which is abundant in the intestinal epithelium, and initiates the production of INFs and cytokines to activate macrophages and neutrophils. The cytokines activate the two intercellular pathways mentioned, JAK\/STAT and NF-\u03baB, and promote leukocyte recruitment, thereby amplifying inflammation. At this point, the intestinal mucosa may suffer epithelial damage, T cells may be activated, and interleukin-17 may be produced. In cases of pre-existing IBD, this systemic activation risks triggering flare-ups and worsening mucosal inflammation (37).<\/p>\n

The studies cited, therefore, have highlighted how shared inflammatory pathways can create a network of bidirectional influence between the two conditions and, in particular, how COVID-19 infection can worsen GI disorders due to psychological factors and the cytokine storm triggered by the virus.<\/p>\n

 <\/p>\n

CONCLUSIONS<\/strong><\/p>\n

 <\/p>\n

The literature contains many studies investigating the exacerbation of systemic inflammatory diseases in the post-COVID-19 phase, but further research is needed to confirm the correlation between them and to investigate the inflammatory mechanisms that characterise both conditions. On the other hand, it is clear that systemic health is severely compromised by the infection and its consequences, including persistent inflammation, cytokine storm, autoantibody production, endothelial damage, as well as the psychological stress induced by the pandemic and lockdown. This narrative review provides a useful overview for exploring the correlations between these conditions and SARS-CoV-2 infection.<\/p>\n

 <\/p>\n

Conflict of interest <\/em><\/p>\n

The authors declare that they have no conflict of interest.<\/p>\n

 <\/p>\n

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