Polymorphonuclear leukocytes (PMNL) in bronchoalveolar lavage (BAL) fluid of cystic fibrosis patients express increased levels ofreceptor for the Fe portion ofIgA (FcαR), similar to those found on PMNL stimulated with FMLP in vitro. Since tumor necrosis factor-α (TNFα) is an activator of PMNL and is found at inflammatory sites, its effects on FcαR expression and IgA-mediated PMNL functions were investigated. Exposure of PMNL to TNFα increased surface expression of FcαR 2- to 3-fold, increased superoxide production in response to aggregated IgA 5-fold, and increased phagocytosis of IgA aggregates 3- to 4-fold. Interleukin-8 did not increase FcαR expression and did not enhance IgA-mediated superoxide generation. IgA-dependent PMNL killing of Pseudomonas aeruginosa was enhanced when PMNL were pretreated with TNFα. Thus, interactions between phagocytic host defense mechanisms and mucosal IgA may be enhanced by TNFα in the inflammatory milieu of the cystic fibrosis lung.

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