A previous report showed that hamsters immunized by epicutaneous application of 2,4,6-trinitrochloro-1-benzene (TNCB) were susceptible to the development of pulmonary interstitial
fibrosis (PIF) if challenged in the lung with the water-soluble form of this
hapten 2,4,6-trinitrobenzene sulphonic
acid (TNBS). In this study, we investigated the immunological mechanisms that contributed to increased
collagen content in the lungs of
hapten-immune hamsters after receiving a pulmonary challenge of the sensitizing
hapten trinitrophenol (TNP). In order to evaluate the concept that delayed-type
hypersensitivity (DTH) reaction modulated their response to TNP in the lung such that it eventuated into PIF, we compared the cutaneous DTH response (48 hr after challenge) with lung
collagen deposition (14 days after challenge) in several lines (strains) of hamsters. The inbred LSH strain, was a high responder in the DTH assay to TNP and developed non-resolving PIF in the
hapten-immune animals. This is called
hapten-immune pulmonary interstitial
fibrosis or HIPIF. We also observed that female LSH hamsters were more susceptible to HIPIF induced by TNP than males. On the other hand, age factors influenced DTH and PIF in random-bred LVG hamsters since young hamsters (3 months old) were low responders to TNP and did not develop PIF in the HIPIF model but matured LVG hamsters (retired breeders) possessed DTH reactivity to TNP and subsequently developed PIF. These results suggest that lung
collagen deposition in
hapten-immune hamster is regulated by T-lymphocyte-mediated immune
inflammation (DTH) in the lung and both are dependent on the ability to develop a cutaneous DTH reaction to the
hapten. The elucidation of possible mechanisms of DTH-mediated non-granulomatous, non-resolving PIF is important for understanding of the role of environmental chemicals similar in action to
haptens in the mediation of skin and
lung diseases.