Defective lipopolysaccharide-induced production of both interleukin 1α and interleukin 1β by A/J mouse macrophages is posttranscriptionally regulated

Abstract

Interleukin 1 (IL-1) production by A/J (A) and C57BL/6J (B6) mouse peritoneal macrophages stimulated with lipopolysaccharide (LPS) was determined. Strain A macrophages produced low levels of soluble IL-1 bioactivity compared with B6 macrophages. This defect was not reversed by indomethacin, interferon-gamma, phorbol myristate acetate, or calcium ionophore A23187. In contrast, cytosolic IL-1 bioactivity was similar in LPS-stimulated A and B6 macrophages. Western blotting revealed that A macrophage supernatants contained lower levels of both 17-kd IL-1 alpha and 17-kd IL-1 beta but similar levels of tumor necrosis factor alpha compared with B6 macrophages. Cytosolic levels of 31-kd pro-IL-1 alpha and also 31-kd pro-IL-1 beta were similar in A and B6 macrophages. Oligonucleotide probing indicated that A and B6 macrophages contained similar levels of IL-1 alpha and also IL-1 beta mRNA. These findings indicate that LPS-stimulated A macrophage culture supernatants contain low levels of both IL-1 alpha and IL-1 beta compared with B6 macrophages and that these defects in IL-1 production are posttranscriptionally regulated.

Analysis of cytokine mRNA expression in Listeria-resistant C57BL/6 and Listeria-susceptible A/J mice during Listeria monocytogenes infection

“…These two strains of mice did not differ in expression of mRNA for TNF-a, IL-la, IL-2, and IL-4 in either the spleen or liver, as assessed by both RT-PCR analysis and in situ hybridization. Our results are consistent with a report that macrophages from C57BL/6 and ANJ mice do not differ in their ability to transcribe IL-la and IL-1,B mRNA in response to lipopolysaccharide stimulation in vitro (1). Semiquantitative analysis with 32P-labelled oligonucleotide probes indicated that the resistant C57BL/6 mice expressed greater amounts of IFN--y and GM-CSF mRNAs in the spleen than did susceptible A/J mice (Fig.…”

Susceptibility of different mouse strains to peri‐implantitis

“…Data are mean ± standard error of the mean. ***P < .001, **P < .01, *P < .05 (n ≥ 3 for all groups) present with decreased neutrophil infiltration and diminished acute inflammation, and macrophages from A/J mice express lower levels of interleukin-1 compared with C57BL/6J mice, 27,28 which is consistent with the reduced neutrophil counts observed in A/J mice compared with C57BL/6J mice in the present study after development of PI. As a result of inherent immune and inflammatory host-response differences, and their resistance and susceptibility to PI, A/J, C3H/HeJ and C57BL/6J mice make suitable animal models for understanding the genetic differences that contribute to PI.…”

“…24 In our study, the distinct responses to experimental PI observed among the different strains are most probably a result of inherent differences in immune response and bone modeling/remodeling. For instance, the antagonistic phenotypes observed in A/J and C57BL/6J mice have already been evaluated in many systems, including neutrophil physiology, the inflammatory infiltrate response and the mac- present with decreased neutrophil infiltration and diminished acute inflammation, and macrophages from A/J mice express lower levels of interleukin-1 compared with C57BL/6J mice, 27,28 which is consistent with the reduced neutrophil counts observed in A/J mice compared with C57BL/6J mice in the present study after development of PI. As a result of inherent immune and inflammatory host-response differences, and their resistance and susceptibility to PI, A/J, C3H/HeJ and C57BL/6J mice make suitable animal models for understanding the genetic differences that contribute to PI.…”