Hypersensitivity Pneumonitis

The lower incidence of hypersensitivity pneumonitis in smokers is a well-known clinical association. Blanchet and coworkers examined whether nicotine might be responsible for this effect. Nicotine or vehicle was administered to mice either intranasally or intraperitoneally simultaneously with induction of a model of hypersensitivity pneumonitis. Lung inflammation, as measured by histology or bronchoalveolar lavage cell counts, was reduced in the nicotine-treated mice, as was mRNA for some inflammatory cytokines, including IFN- ${gamma}$ . The authors concluded that nicotine reduces some measures of inflammation in this model and suggest that nicotine treatment of hypersensitivity pneumonitis, as is done in ulcerative colitis, be considered.

Lacasse and coworkers examined whether a clinical prediction rule might be reliable for making a diagnosis of hypersensitivity pneumonitis without the need for bronchoalveolar lavage or biopsy. A cohort of 400 patients (116 with hypersensitivity pneumonitis and 284 control subjects) was recruited. Hypersensitivity pneumonitis was diagnosed on the basis of high-resolution computed tomography, bronchoalveolar lavage, and, if necessary, surgical lung biopsy. Six significant predictors of hypersensitivity pneumonitis were identified: (i) exposure to a known offending antigen, (ii) positive precipitating antibodies to the offending antigen, (iii) recurrent symptoms, (iv) inspiratory crackles, (v) symptoms within 4 to 8 hours of exposure, and (vi) weight loss. The area under a receiver operating characteristic curve was 0.93 for the clinical prediction rule. The rule retained its accuracy when validated in a separate cohort of 261 patients. The authors conclude that a clinical decision rule, not requiring bronchoalveolar lavage or biopsy, is reliable in the diagnosis of hypersensitivity pneumonitis, especially in areas of high or low prevalence. An editorial commentary by Morris accompanies this article.

The most common form of hypersensitivity pneumonitis in Japan is summer-type hypersensitivity pneumonitis, which is caused by inhalation of Trichosporon asahii or Trichosporon mucoides. To determine what proteins are involved in the pathogenesis, Matsunaga and coworkers constructed a cDNA expression library of T. asahii. They identified and cloned a novel gene encoding a 19-kD protein, named TA-19. IgG, IgA, and IgM antibodies to the recombinant TA-19 protein were higher in serum and bronchoalveolar lavage fluid in patients than in control subjects. The protein induced pneumonitis-specific proliferation of mononuclear cells from both the peripheral blood and bronchoalveolar fluid. The authors conclude that a novel gene, TA-19, derived from Trichosporon asahii modulates cellular and immune responses of patients with summer-type hypersensitivity pneumonitis.

Citations 1-4 of 4 total displayed.

Inhibitory Effect of Nicotine on Experimental Hypersensitivity Pneumonitis In Vivo and In Vitro

Marie-Renée Blanchet, Evelyne Israël-Assayag, and Yvon Cormier
Am. J. Respir. Crit. Care Med. 169: 903 -909. First published online as doi:10.1164/rccm.200210-1154OC [Abstract] [Full text]

Gold, Silver, and Bronze: Metals, Medals, and Standards in Hypersensitivity Pneumonitis

David G. Morris
Am. J. Respir. Crit. Care Med. 168: 909-910. [Full text]

Clinical Diagnosis of Hypersensitivity Pneumonitis

Yves Lacasse, Moises Selman, Ulrich Costabel, Jean-Charles Dalphin, Masayuki Ando, Ferran Morell, Riitta Erkinjuntti-Pekkanen, Nestor Müller, Thomas V. Colby, Mark Schuyler, and Yvon Cormier
Am. J. Respir. Crit. Care Med. 168: 952 -958. First published online as doi:10.1164/rccm.200301-137OC [Abstract] [Full text]

TA-19, a Novel Protein Antigen of Trichosporon asahii, in Summer-type Hypersensitivity Pneumonitis

Yasujiro Matsunaga, Yutaka Usui, and Yasuyuki Yoshizawa
Am. J. Respir. Crit. Care Med. 167: 991 -998. First published online as doi:10.1164/rccm.200206-589OC [Abstract] [Full text]

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