Skip to main content
NCBI home page
Immunology logoLink to Immunology
. 1987 Jun;61(2):215–219.

Desensitization of the acute inflammatory response in skin and mammary gland of sheep.

P J Maas, I G Colditz
PMCID: PMC1453386  PMID: 3596638

Abstract

Desensitization of the inflammatory response was investigated in the mammary glands and skin of sheep. Following twice daily stimulation of non-lactating glands, neutrophil concentrations in inflammatory exudates during the seventh response to endotoxin (1 microgram) and zymosan-activated plasma (1 ml) were 30% and 20% and those in primary responses occurring concurrently in contralateral glands. Cross-desensitization of ZAP was found in non-lactating glands pretreated with endotoxin. In lactating glands, inflammatory responses were examined following daily infusion of endotoxin (1 microgram) and oyster glycogen (50 mg). The neutrophil influx following infusion of each agent declined linearly, with the fourth response being 16% of the first response for both agents. On Day 5, inflammatory responses in contralateral glands receiving an initial challenge were comparable with primary responses on Day 1 in repeatedly stimulated glands. Thus, desensitization was a local phenomenon restricted to the restimulated gland. The return of normal responsiveness to 1 microgram endotoxin occurred after 9 days in glands desensitized by infusion of a single dose of 50 micrograms endotoxin. Accumulation of neutrophils and leakage of plasma were examined in skin sites restimulated with endotoxin and oyster glycogen. Neutrophil accumulation in restimulated lesions was comparable to primary lesions after about 3.5 days for endotoxin and 4.5 days for oyster glycogen. On the other hand, plasma leakage did not return to normal until Day 8 for endotoxin and until after Day 10 for oyster glycogen. The dissociation between neutrophil accumulation and plasma leakage in restimulated skin lesions contrasts with the dependence of plasma leakage on neutrophil migration reported in primary inflammatory lesions. The results suggest that desensitization of the inflammatory response may influence the pathogenesis of bacterial infection.

Full text

PDF
215

Selected References

These references are in PubMed. This may not be the complete list of references from this article.

  1. Carlson G. P., Kaneko J. J. Isolation of leukocytes from bovine peripheral blood. Proc Soc Exp Biol Med. 1973 Mar;142(3):853–856. doi: 10.3181/00379727-142-37131. [DOI] [PubMed] [Google Scholar]
  2. Colditz I. G. Kinetics of tachyphylaxis to mediators of acute inflammation. Immunology. 1985 May;55(1):149–156. [PMC free article] [PubMed] [Google Scholar]
  3. Colditz I. G., Movat H. Z. Chemotactic factor-specific desensitization of skin to infiltration by polymorphonuclear leukocytes. Immunol Lett. 1984;8(2):83–87. doi: 10.1016/0165-2478(84)90055-5. [DOI] [PubMed] [Google Scholar]
  4. Colditz I. G., Movat H. Z. Desensitization of acute inflammatory lesions to chemotaxins and endotoxin. J Immunol. 1984 Oct;133(4):2163–2168. [PubMed] [Google Scholar]
  5. Colditz I. G., Watson D. L. The immunophysiological basis for vaccinating ruminants against mastitis. Aust Vet J. 1985 May;62(5):145–153. doi: 10.1111/j.1751-0813.1985.tb07276.x. [DOI] [PubMed] [Google Scholar]
  6. Craven N., Williams M. R. Defences of the bovine mammary gland against infection and prospects for their enhancement. Vet Immunol Immunopathol. 1985 Oct;10(1):71–127. doi: 10.1016/0165-2427(85)90039-x. [DOI] [PubMed] [Google Scholar]
  7. Issekutz A. C., Movat K. W., Movat H. Z. Enhanced vascular permeability and haemorrhage-inducing activity of rabbit C5ades arg: probable role of polymorphonuclear leucocyte lysosomes. Clin Exp Immunol. 1980 Sep;41(3):512–520. [PMC free article] [PubMed] [Google Scholar]
  8. MILES A. A., MILES E. M. Vascular reactions to histamine, histamine-liberator and leukotaxine in the skin of guinea-pigs. J Physiol. 1952 Oct;118(2):228–257. doi: 10.1113/jphysiol.1952.sp004789. [DOI] [PMC free article] [PubMed] [Google Scholar]
  9. Normann S. J., Schardt M., Sorkin E. Antileukocyte activity I. Systemic inhibition of cellular emigration following local inflammation. J Leukoc Biol. 1985 Mar;37(3):319–330. doi: 10.1002/jlb.37.3.319. [DOI] [PubMed] [Google Scholar]
  10. Oyvin I. A., Gaponiuk P. Y., Oyvin V. I. The effect of bradykinin on permeability of skin blood vessels. Experientia. 1967 Nov 15;23(11):925–926. doi: 10.1007/BF02136224. [DOI] [PubMed] [Google Scholar]
  11. Paape M. J., Pearson R. E., Wergin W. P., Guidry A. J. Enhancement of chemotactic response of polymorphonuclear leukocytes into the mammary gland and isolation from milk. J Dairy Sci. 1977 Jan;60(1):53–62. doi: 10.3168/jds.S0022-0302(77)83828-9. [DOI] [PubMed] [Google Scholar]
  12. Smith K. L., Todhunter D. A., Schoenberger P. S. Environmental mastitis: cause, prevalence, prevention. J Dairy Sci. 1985 Jun;68(6):1531–1553. doi: 10.3168/jds.S0022-0302(85)80993-0. [DOI] [PubMed] [Google Scholar]
  13. Wedmore C. V., Williams T. J. Control of vascular permeability by polymorphonuclear leukocytes in inflammation. Nature. 1981 Feb 19;289(5799):646–650. doi: 10.1038/289646a0. [DOI] [PubMed] [Google Scholar]

Articles from Immunology are provided here courtesy of British Society for Immunology

RESOURCES