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M Parant

Publications and source records attributed to M Parant.

103 records · Page 6Linked to original sources
PubMedDate not supplied

Stimulation of non-specific resistance to infections by synthetic immunoregulatory agents.

Muramyl dipeptide or MDP (AcMur-L-Ala-D-iGln) is a synthetic immunoadjuvant which can also enhance non-specific resistance to bacterial infections in mice, even by the oral route. By the use of several derivatives, it has been shown that neither adjuvanticity nor pyrogenicity was a perequisite for eliciting an increased resistance, and that unwanted pharmacological effects can be eliminated by minor chemical modifications. Moreover, some lipophilic analogs or derivatives obtained by linking the glycopeptide to a carrier were found to be more active than MDP. Their effectiveness also depended on the dose and the timing of administration, and varied according to the bacterial challenge. The most appropriately timed administration of MDP and derivatives was established between one and four days before the challenge. In some cases, MDP was protective even when injected one hour after the challenge, whereas with other immunostimulants such as lipopolysaccharides or BCG, a negative phase of higher susceptibility may occur under these conditions. MDP still enhanced resistance to bacterial infections in animals with a poor immune status, like newborns or adult mice under immunosuppressive treatment. Moreover, the protective activity was not impaired after repeated injections of large doses of MDP or other adjuvant analogs, a treatment which is known to inhibit specific immune responses.

Acetylmuramyl-Alanyl-Isoglutamine↗
PubMedDate not supplied

[Non-specific responses of C3H/He low responder mice to LPS and to TCA-extracted endotoxin].

In vitro and in vivo host reponses to lipopolysaccharide (LPS) and various immunostimulants were compared in C3h low-and highresponder mice, their F1, F2 and backcross hybrids. In contrast to the responsiveness of a congeneic high responder subline, LPS is unable to stimulate thymidine incorporation by splenocytes of the low-responder subline and to protect these mice against an unrelated bacterial infection, Moreover, although endotoxin extracted by trichloroacetic acid was mitogenic in these low-responder mice, it was still unable to increase their resistance against an infectious challenge; in addition, the LD50 of both endotoxin preparations was about 3,500 fold greater than in the high-responder mice. For this latter assay, mice were adrenaloctomized since it is well established that mouse's susceptibility to LPS is dramatically enhanced in the absence of glucocorticoids. Inheritance of susceptibility to lethal effect of endotoxin and of LPS-induced non-specific resistance to infection was also tested in both sublines, their hybrids and backcross progeny. The present findings are consistent with the hypothesis that these LPS host-responses may be determined by a single autosomal dominant gene.

Animals↗