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Organs at different anatomic sites of the body have vastly different physiological functions and face dramatically different microbial challenges on a daily basis. These factors help shape each organ's unique and customized immune response to infection. Organ-specific immunity ensures that, during infection, an effective immune response is launched, while excessive inflammation and immunopathology are minimized. Peng and Monack (p. 2723-2733) show that an immune molecule with dual antimicrobial and immunoregulatory roles, indoleamine 2,3-dioxygenase 1, is induced specifically in infected lungs and inhibits the growth of Francisella tularensis tryptophan auxotrophs. This work demonstrates the importance of organ-specific immune mechanisms that affect microbial metabolic requirements for colonization of specific organs.
Sepsis results from an alteration in pro- and anti-inflammatory cytokine production in response to invading organisms. The mitogen-activated protein kinase (MAPK) pathway is a key signal transduction pathway involved in cytokine production in sepsis, and its regulation is incompletely understood. Cornell and colleagues (p. 2868-2876) show that the dual-specific phosphatase MAPK phosphatase 2 (MKP-2) is a key regulator of the MAPK pathway in sepsis, in that in MKP-2−/− mice have less cytokine production than and a survival advantage over wild-type mice. MKP-2's regulatory mechanism seems to involve both extracellular-regulated protein kinase and another phosphatase, MAPK phosphatase 1.
Chlamydia trachomatis is the etiological agent of blinding trachoma and sexually transmitted infections. Comparative genomics have implicated genes within the chlamydial plasticity zone as important virulence factors that influence human infection tropism and immune evasion. Taylor and colleagues (p. 2691-2699) describe the biological characterization of the C. trachomatis specific plasticity zone protein CT153, a MACPF domain protein. CT153 was shown to be common to all human C. trachomatis serovars and was proteolytically cleaved following early interactions of the organism with host cells. These findings implicate an important biological function for CT153 in the pathogenesis of chlamydial infection.