"Alox5" Gene knockout mice are more susceptible to the development and pathological complications of experimental infection with "Klebsiella pneumoniae", "Borrelia burgdorferi", and Paracoccidioides brasiliensis. In a model of cecum perforation-induced sepsis, "ALOX5" gene knockout mice exhibited a decrease in the number of neutrophils and an increase in the number of bacteria that accumulated in their peritoneum. On the other hand, ALOX5 gene knockout mice demonstrate an enhanced resistance and lessened pathology to Brucella abortus infection and, at least in its acute phase, Trypanosoma cruzi infection. Furthermore, "Alox5"-null mice exhibit a worsened inflammatory component, failure to resolve inflammation-related responses, and decreased survival in experimental models of respiratory syncytial virus disease, Lyme disease, Toxoplasma gondii disease, and corneal injury. These studies indicate that Alox5 can serve a protective function presumably by generating metabolites such as chemotactic factors that mobilize the innate immunity system. However, the suppression of inflammation appears also to be a function of Alox5, presumably by contributing to the production of anti-inflammatory specialized pro-resolving mediators (SPMs), at least in certain rodent inflammation-based model systems. These genetic studies allow that ALOX5 along with the chemotactic factors and SPMs that they contribute to making may play similar opposing pro-inflammatory and anti-inflammatory functions in humans.