ABSTRACT
Fundamentally, the pathophysiology of enteritis and colitis is inflammatory in nature, and the clinical abnormalities that we associate with these conditions, such as enterogastric reflux and diarrhea, arise from the inflammatory processes involving the affected segment of the gastrointestinal tract. The initial stages of these conditions typically involve localized mucosal inflammation, but this frequently progresses to widespread systemic activation of the inflammatory cascade. Many of the sequelae of these conditions, such as laminitis and multiple organ failure, are related to this systemic inflammatory response.
Inflammation Inflammation represents the response of tissues either to injury or the presence of microorganisms. Inflammation serves a vital role in the host’s resistance to infection, as it enhances the directed movement of phagocytic cells and defensive molecules, such as immunoglobulin and complement, from the bloodstream to the site of infection or injury. Local inflammation arises as a result of several different insults, including direct mucosal cellular injury by the pathogen, the elaboration of toxins that injure the mucosal cells, and the production of inflammatory mediators by the host tissue in response to the presence of the pathogen or its toxins. Direct cellular injury requires that the pathogens gain access to the host’s intestinal tissue, either from the luminal surface or by hematogenous spread. Once an organism has gained access to the host cell, it may invade the cell and establish an intracellular infection, as is the case with Salmonella sp. organisms, or it may liberate enzymes, toxins, or other substances that damage the host cell. Injured cells release preformed mediators such as histamine and synthesize proinflammatory substances, including eicosanoids (prostaglandins, thromboxanes, leukotrienes) and the cytokines IL-1 and TNF-α. These mediators are responsible for the initiation of a nonspecific inflammatory response. The bacterial cellular components that are recognized by the immune system include endotoxin (lipopolysaccharide, LPS) and exotoxins from gram-negative bacteria, and peptidoglycan (PG), lipoteichoic acids (LTA), enterotoxins, or superantigenic exotoxins from gram-positive bacteria.1,2 It is important to note that while bacterial infection may be responsible for the initiation of an inflammatory response, the inflammatory process itself results solely from the production of endogenous mediators.
