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Effects of aging on exocrine immune responses to Mycoplasma pulmonis

, : Effects of aging on exocrine immune responses to Mycoplasma pulmonis. Mechanisms Of Ageing & Development. 66(2): 131-147

Formalinized Mycoplasma pulmonis was used to immunize 3 different age groups of Fischer 344 rats. A specific antibody to this antigen was detected in both saliva and lung lavage fluids and differences were noted in the elicitation of secretory antibody between the different ages of the animals. Few statistical differences were noted between the three age groups for salivary IgG responses to M. pulmonis, regardless of the dosage given, even though all responses were greater than their respective control groups. The principal differences among the three age groups were noted in the kinetics of the response, that is, the amount of time that was necessary to produce a peak response. The younger group of animals took less time to produce a peak response than the older two groups, even though the magnitude of the response was lower. Salivary IgA responses to M. pulmonis appeared predominantly as a primary response, particularly in the senescent animals. Secondary salivary IgA responses were not significantly greater than their respective primary responses, suggesting that secretory IgA did not display classic anamnestic responses that were observed with salivary IgG. As with IgG responses, the senescent animals took longer to produce a peak salivary IgA response when compared to the other age groups. Lung lavage IgG responses, normalized to total protein, were greatest in the youngest group of animals and appeared to diminish as the age of the animal increased. In contrast, lung lavage IgA responses to M. pulmonis were of a greater magnitude in the senescent animals. These studies suggest that senescent animals are capable of eliciting a humoral immune response in mucosal secretions to Mycoplasma pulmonis. However, differences noted with regard to disease severity and mortality to respiratory mycoplasmosis in senescent animals may result from intrinsic defects in the quality of the humoral response or as a consequence of deficient cellular responses to this pathogen.


PMID: 1365840

DOI: 10.1016/0047-6374(92)90131-v

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