Airway hyperresponsiveness is a key feature of asthma, but its mechanisms remain poorly understood. Leukotriene D(4) (LTD(4)) is one of the few molecules capable of producing airway hyperresponsiveness. In this study, LTD(4), but not leukotriene C(4) (LTC(4)), produced a leftward displacement of the concentration-response curve to histamine in bovine airway smooth muscle strips. Neither LTC(4) nor LTD(4) modified the concentration-response curve to carbachol. In simultaneous measurements of intracellular Ca(2+) ([Ca(2+)](i)) and contraction, histamine or carbachol produced a transient Ca(2+) peak followed by a plateau, along with a contraction. LTD(4) increased the histamine-induced transient Ca(2+) peak and contraction but did not modify responses to carbachol. Enhanced responses to histamine induced by LTD(4) were not modified by staurosporine or chelerythrine but were abolished by genistein. Western blot showed that carbachol, but not histamine, caused intense phosphorylation of extracellular signal-regulated kinase 1/2 and that LTD(4) significantly enhanced the phosphorylation induced by histamine, but not by carbachol. L-type Ca(2+) channel participation in the hyperresponsiveness to histamine was discarded because LTD(4) did not modify the [Ca(2+)](i) changes induced by KCl. In tracheal myocytes, LTD(4) enhanced the transient Ca(2+) peak induced by histamine (but not by carbachol) and the sarcoplasmic reticulum (SR) Ca(2+) refilling. Genistein abolished this last LTD(4) effect. Partial blockade of the SR-ATPase Ca(2+) pump with cyclopiazonic acid reduced the Ca(2+) transient peak induced by histamine but not by carbachol. These results suggested that LTD(4) induces hyperresponsiveness to histamine through activation of the tyrosine kinase pathway and an increasing SR-ATPase Ca(2+) pump activity. L-type Ca(2+) channels seemed not to be involved in this phenomenon.

Our data suggested that beta1-integrin shedding produced by repetitive allergen challenges in guinea-pigs was associated with collagen deposition in SER of bronchi and bronchioles, along with inflammatory cells infiltration and AI-AHR development.

The authors' objective was to study the presence of IgM antiavian antibodies in sera from patients with pigeon breeder’s disease. We studied 93 patients with interstitial lung disease admitted for the assessment of pigeon breeder's disease. Eighty sera from healthy donors with no history of bird contact and 47 asymptomatic pigeon breeders were included as controls. The presence of IgM, IgG, and IgA antiavian antibodies was detected by ELISA and Western blot using avian‐pooled serum antigen. Fifty‐three patients were classified as having definite pigeon breeder's disease, whereas 40 did not fulfill these diagnostic criteria. The levels of IgM antiavian‐antibodies in pigeon breeder’s disease by ELISA exceeded both the values of healthy subjects with no history of avian contact (P = 2.5 × 10–8) and the results of asymptomatic breeders (P = 0.03). Positive IgA antiavian antibodies were the most frequent abnormalities in pigeon breeder's disease showing values over the reference levels of control groups that reach significant statistical differences. Both precipitin‐positive and ‐negative samples demonstrated IgM reactivity. IgM antiavian antibodies were confirmed by Western blot. A relationship of IgM positive tests with a recent history of avian antigen exposure and acute disease was found. Additionally, the positive IgM group included patients having subacute and chronic lung disease. Antiavian antibodies have previously been considered of minor significance in hypersensitivity pneumonitis; nevertheless, recent studies support their use in clinical diagnosis. Although no specific laboratory tests can confirm the diagnosis in pigeon breeder’s disease, IgM antiavian antibodies may be useful for detecting recent antigen exposure and the acute stage of the disease. J. Clin. Lab. Anal. 14:201–207, 2000. © 2000 Wiley‐Liss, Inc.

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No single immunological test may definitively distinguish pigeon HP from AB and other interstitial lung disorders; however, positive RF, together with high AA levels, seems to be useful in differentiating the diagnosis.