Inflammation is a biological response of the immune system that can be triggered by a variety of factors, including pathogens, damaged cells and toxic compounds. These factors may induce acute and/or chronic inflammatory responses in the heart, pancreas, liver, kidney, lung, brain, intestinal tract and reproductive system, potentially leading to tissue damage or disease. 

Both infectious and non-infectious agents and cell damage activate inflammatory cells and trigger inflammatory signalling pathways.


To prevent progression from acute inflammation to persistent, chronic inflammation, the inflammatory response must be suppressed to prevent additional tissue damage. 

Chronic inflammation occurs when acute inflammatory mechanisms fail to eliminate tissue injury [1], and may lead to a host of diseases, such as cardiovascular diseases, atherosclerosis, type 2 diabetes, rheumatoid arthritis and cancers [2]. Understanding the common mechanisms that orchestrate dysfunction in the various organ systems will allow for development and production of improved targeted therapies.


Inflammation has long been recognized as a major cause of disease. It is estimated that some 15% of human cancers are associated with chronic infection and inflammation [3]. Acute and chronic inflammation-mediated tissue injury is observed in many organ systems, including the heart, pancreas, liver, kidney, lung, brain, intestinal tract and reproductive system.


Cardiovascular disease and its underlying pathology, atherosclerosis, is the major cause of death and disability worldwide [4, 5]. By 2030, almost 23.6 million people are projected to die annually from cardiovascular disorders [6, 7]. Inflammatory mediators play key roles in atherosclerosis, from initial leukocyte recruitment through rupture of the atherosclerotic plaque [8–11]. Inflammation is also an early event in cardiac stress. Elevated levels of endothelial adhesion molecules and increased inflammatory cytokine and chemokine (small cytokines, or signalling proteins secreted by cells) production and release are observed in affected cardiac tissues [12].

The innate immune system is the primary cardiac defense against pathogens and tissue damage [13]. Myocardial infarction, which commonly results from coronary atherosclerosis and involves acute loss of many myocardial cells, is the most common cause of cardiac injury [14]. 

Cardiovascular disease is the main cause of death and disability in patients with diabetes mellitus, especially those with type 2 diabetes (T2D), in whom cardiovascular disease occurs 14.6 years earlier on average [15]. About two-thirds of deaths in people with diabetes are due to cardiovascular disease; among these, approximately 40% die from ischemic heart disease, 15% from other forms of heart disease, principally congestive heart failure, and about 10% from stroke [16]. Recent global estimates indicate that over 422 million adults currently live with diabetes, of which over 90% have T2D.

Diabetes is a group of metabolic disorders characterized by sustained high blood sugar levels, and is a major global health challenge, both to individuals and their families, and to healthcare systems [17]. Diabetes complications include heart attack, stroke, kidney failure, limb amputation, blindness and nerve damage.


Pancreatic cancer (PC) remains one of the most lethal of malignancies and a major health burden [18], and is the fourth most common cause of death from cancer in the US [19].


Inflammation in the liver protects this organ from infection and injury, but excessive inflammation may lead to extensive loss of hepatocytes, ischemia-reperfusion injury, metabolic alterations, and eventually permanent hepatic damage [20]. Inflammation can destroy hepatic parenchymal cells, increasing the risk of chronic liver diseases, such as non-alcoholic fatty liver disease (NAFLD) or viral hepatitis. Chronic liver diseases are a leading cause of morbidity and mortality in the US [21].


Lung inflammatory diseases involve complex interactions among and between structural and immune cells [22]. Lung inflammation results predominantly from tissue exposure to bacterial and viral pathogens and/or environmental pollutants. Excessive acute inflammation and subsequent lung injury can cause pulmonary fibrosis and impair gas exchange. Unresolved lung injury and chronic inflammation are frequently observed in acute respiratory distress syndrome, cystic fibrosis, chronic obstructive pulmonary disease (COPD) and asthma [23–25].


Kidney inflammation contributes to progressive renal injury, which may lead to glomerulonephritis, end-stage renal disease or acute or chronic kidney disease (CKD) [26–28]. Approximately 10–12% of the population suffer from CKD, and some 50% of elderly patients show signs of kidney dysfunction, which is associated with high morbidity and mortality [29]. Kidney inflammation is most commonly induced by infection, ischemia/reperfusion, in situ immune-complex formation/deposition, or complement pathway dysregulation [26]. CKD and acute kidney injury (AKI) are the most severe types of kidney disease [30].

Intestinal Tract

Acute and chronic inflammatory diseases of the intestine can cause various health issues, and decrease patient quality of life [31, 32]. The complex, polygenetic inflammatory bowel diseases (IBDs) are characterized by an excessive inflammatory response to gut lumen (epithelial membrane, part of the intestinal structure) microbial flora [33]. IBDs mainly include ulcerative colitis (UC) and Crohn’s disease (CD), but also non-infectious inflammation of the bowel [34, 35].

Reproductive System

The hallmarks of inflammation are observed during many normal reproductive processes, including menstruation, ovulation, implantation and childbirth [36]. Injury and healing caused by menstruation, ovulation and childbirth trigger the inflammatory cascade. However, initiation and maintenance of inflammatory processes are also important components of many reproductive tract diseases.


Inflammatory responses occur in the brain in many central nervous system (CNS) diseases, including autoimmune diseases, neurodegenerative diseases like Alzheimer’s (AD) and Parkinson’s disease (PD) and epilepsy. Inflammatory responses in the brain can enhance neuronal excitability, injure cells and increase blood-brain barrier permeability to various molecules [37–39].


Inflammation is frequently a key element in the pathological progression of organ disease. Three main pathways play major roles in inflammation, and dysregulation of one or more of these pathways can lead to inflammation-associated disease.

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