Lymphocytes in non-immune inflammation: a specific subclass of lymphoid cells?

Rats were subjected to various experimental procedures which affected lymphocyte numbers, in an attempt to investigate the participation of individual subpopulations of these cells in the development of acute, non-immune inflammation. Deficient T function, as evidenced in neonatally thymectomized animals, or in 6-week-old animals thymectomized and afterwards exposed to multiple total-body X-ray irradiations, did not interfere with the development of the acute inflammatory responses of the animals to carrageenin. In the former circumstance, the numbers of circulating B lymphocytes, identified by the presence of surface immunoglobulins, were increased. In thymectomized and irradiated rats, the B-lymphocyte subpopulation was reduced. Circumstances causing attenuated inflammatory reactions to carrageenin resulted, first, from lymphocyte depletion by chronic drainage from the thoracic duct and, second, from irradiation of the animals with a single large dose of X-ray, the animals being tested 24 h after irradiation. B lymphocytes in blood remained within the normal range after chronic lymphatic drainage, but a large dose of X-ray markedly reduced their number. In both cases the attenuation of the responses to carrageenin did not seem to be associated with nonspecific hyporeactivity, or with the effect of the treatments on the other blood cells, It is suggested that the development of acute, non-immune inflammation is influenced by lymphoid cells which might constitute a specific subclass of cells, distinct from fully differentiated T and B lymphocytes.

Acute inflammatory responses in rats with protein-calorie malnutrition.

An animal model of protein-calorie malnutrition (PCM) was produced by keeping rats on a protein-free diet during the 13-day interval which followed the period of normal lactation. Malnutrition was characterized by reduction in body weight, in plasma proteins, cholesterol, haemoglobin and leucocyte counts, relative to controls from the same litter receiving a balanced diet. Acute inflammatory responses induced in these animals by carrageenin or staphylococci suspensions, differed markedly from those evoked in matching controls: the resulting oedema developed more slowly and yet persisted for longer intervals; Evans blue, injected i.v., leaked into the inflamed areas in smaller quantities; reduced cell migration to the site of the lesion was observed. The slow development of the response was attributed to the decreased levels of circulating proteins and its persistency to a defective drainage of exuded material. It is concluded that PCM can impair the capacity of response to noxious stimuli, thus rendering the animals more susceptible to infections.