Collagen-induced arthritis and pregnancy in mice: The effects of pregnancy on collagen-induced arthritis and the high incidence of infertility in arthritic female mice

F. Hirahara, P. H. Wooley, H. S. Luthra, C. B. Coulam, M. M. Griffiths, C. S. David

Research output: Contribution to journalArticle

22 Citations (Scopus)

Abstract

Collagen-induced arthritis (CIA) in mice is a model of inflammatory polyarthritis that has many features similar to human rheumatoid arthritis. In rheumatoid arthritis, pregnancy leads to amelioration of the disease while exacerbation develops after delivery. We used the CIA model to elucidate the role of pregnancy on disease and vice versa. The onset of arthritis in pregnant mice was delayed in the B10.RIII strains immunized with native porcine type II collagen 7-12 days prior to syngeneic [B10.RIII (susceptible to CIA) x B10.RIII] and allogeneic (B10.RIII female x B10.K male that are CIA resistant) pregnancy. In contrast, when mice were immunized on days 1-6 of pregnancy, the onset of arthritis was earlier as compared wtih controls. In addition, once the mice developed CIA after delivery, the disease showed markedly rapid progression as compared to the control immunized group. Humoral immune responses to type II collagen showed significantly decreased levels on day 14 (at late stage of pregnancy) both in syngeneic and allogeneic postmating immunized pregnant mice. The same effect was also seen in allogeneic premating immunized pregnant mice on day 21 (at mid-stage of pregnancy). The levels of these antibodies increased after delivery. Subclasses of IgG1 and IgG(2a) antibodies to type II collagen were suppressed during pregnancy. In the pseudopregnant group, these antibodies showed deceased levels on day 14, but did not differ from the control groups on day 21 and 28. Some immunoregulatory changes may play a role in these alterations in pregnant arthritic mice. In comparison to the effects of syngeneic (susceptible x susceptible) pregnancy on CIA, allogeneic (susceptible female x resistant male) pregnancy seemed to be beneficial for the affected individuals. Litter size and mean birth weight were not affected by immunization of type II collagen. After onset of CIA, both syngeneic and allogeneic matings failed to produce offspring in arthritic female mice. The estrus cyclicity was highly disturbed in arthritic female mice and gonadotropin stimulation in arthritic mice induced significantly less ova in oviducts and maturing follicles as compared to nonarthritic controls. Immunological factors yet to be elucidated may be involved in this ovarian dysfunction.

Original languageEnglish (US)
Pages (from-to)44-54
Number of pages11
JournalAmerican Journal of Reproductive Immunology and Microbiology
Volume11
Issue number2
StatePublished - 1986

Fingerprint

Experimental Arthritis
Infertility
Arthritis
Pregnancy
Incidence
Collagen Type II
Antibodies
Rheumatoid Arthritis
Immunoglobulin G
Collagen Type VII
Litter Size
Control Groups
Oviducts
Estrus
Immunologic Factors
Periodicity
Humoral Immunity
Gonadotropins
Birth Weight
Ovum

ASJC Scopus subject areas

  • Immunology
  • Obstetrics and Gynecology

Cite this

Collagen-induced arthritis and pregnancy in mice : The effects of pregnancy on collagen-induced arthritis and the high incidence of infertility in arthritic female mice. / Hirahara, F.; Wooley, P. H.; Luthra, H. S.; Coulam, C. B.; Griffiths, M. M.; David, C. S.

In: American Journal of Reproductive Immunology and Microbiology, Vol. 11, No. 2, 1986, p. 44-54.

Research output: Contribution to journalArticle

@article{47312bc8fefc48a2a1efbf42846acbcb,
title = "Collagen-induced arthritis and pregnancy in mice: The effects of pregnancy on collagen-induced arthritis and the high incidence of infertility in arthritic female mice",
abstract = "Collagen-induced arthritis (CIA) in mice is a model of inflammatory polyarthritis that has many features similar to human rheumatoid arthritis. In rheumatoid arthritis, pregnancy leads to amelioration of the disease while exacerbation develops after delivery. We used the CIA model to elucidate the role of pregnancy on disease and vice versa. The onset of arthritis in pregnant mice was delayed in the B10.RIII strains immunized with native porcine type II collagen 7-12 days prior to syngeneic [B10.RIII (susceptible to CIA) x B10.RIII] and allogeneic (B10.RIII female x B10.K male that are CIA resistant) pregnancy. In contrast, when mice were immunized on days 1-6 of pregnancy, the onset of arthritis was earlier as compared wtih controls. In addition, once the mice developed CIA after delivery, the disease showed markedly rapid progression as compared to the control immunized group. Humoral immune responses to type II collagen showed significantly decreased levels on day 14 (at late stage of pregnancy) both in syngeneic and allogeneic postmating immunized pregnant mice. The same effect was also seen in allogeneic premating immunized pregnant mice on day 21 (at mid-stage of pregnancy). The levels of these antibodies increased after delivery. Subclasses of IgG1 and IgG(2a) antibodies to type II collagen were suppressed during pregnancy. In the pseudopregnant group, these antibodies showed deceased levels on day 14, but did not differ from the control groups on day 21 and 28. Some immunoregulatory changes may play a role in these alterations in pregnant arthritic mice. In comparison to the effects of syngeneic (susceptible x susceptible) pregnancy on CIA, allogeneic (susceptible female x resistant male) pregnancy seemed to be beneficial for the affected individuals. Litter size and mean birth weight were not affected by immunization of type II collagen. After onset of CIA, both syngeneic and allogeneic matings failed to produce offspring in arthritic female mice. The estrus cyclicity was highly disturbed in arthritic female mice and gonadotropin stimulation in arthritic mice induced significantly less ova in oviducts and maturing follicles as compared to nonarthritic controls. Immunological factors yet to be elucidated may be involved in this ovarian dysfunction.",
author = "F. Hirahara and Wooley, {P. H.} and Luthra, {H. S.} and Coulam, {C. B.} and Griffiths, {M. M.} and David, {C. S.}",
year = "1986",
language = "English (US)",
volume = "11",
pages = "44--54",
journal = "American Journal of Reproductive Immunology",
issn = "1046-7408",
publisher = "Wiley-Blackwell",
number = "2",

}

TY - JOUR

T1 - Collagen-induced arthritis and pregnancy in mice

T2 - The effects of pregnancy on collagen-induced arthritis and the high incidence of infertility in arthritic female mice

AU - Hirahara, F.

AU - Wooley, P. H.

AU - Luthra, H. S.

AU - Coulam, C. B.

AU - Griffiths, M. M.

AU - David, C. S.

PY - 1986

Y1 - 1986

N2 - Collagen-induced arthritis (CIA) in mice is a model of inflammatory polyarthritis that has many features similar to human rheumatoid arthritis. In rheumatoid arthritis, pregnancy leads to amelioration of the disease while exacerbation develops after delivery. We used the CIA model to elucidate the role of pregnancy on disease and vice versa. The onset of arthritis in pregnant mice was delayed in the B10.RIII strains immunized with native porcine type II collagen 7-12 days prior to syngeneic [B10.RIII (susceptible to CIA) x B10.RIII] and allogeneic (B10.RIII female x B10.K male that are CIA resistant) pregnancy. In contrast, when mice were immunized on days 1-6 of pregnancy, the onset of arthritis was earlier as compared wtih controls. In addition, once the mice developed CIA after delivery, the disease showed markedly rapid progression as compared to the control immunized group. Humoral immune responses to type II collagen showed significantly decreased levels on day 14 (at late stage of pregnancy) both in syngeneic and allogeneic postmating immunized pregnant mice. The same effect was also seen in allogeneic premating immunized pregnant mice on day 21 (at mid-stage of pregnancy). The levels of these antibodies increased after delivery. Subclasses of IgG1 and IgG(2a) antibodies to type II collagen were suppressed during pregnancy. In the pseudopregnant group, these antibodies showed deceased levels on day 14, but did not differ from the control groups on day 21 and 28. Some immunoregulatory changes may play a role in these alterations in pregnant arthritic mice. In comparison to the effects of syngeneic (susceptible x susceptible) pregnancy on CIA, allogeneic (susceptible female x resistant male) pregnancy seemed to be beneficial for the affected individuals. Litter size and mean birth weight were not affected by immunization of type II collagen. After onset of CIA, both syngeneic and allogeneic matings failed to produce offspring in arthritic female mice. The estrus cyclicity was highly disturbed in arthritic female mice and gonadotropin stimulation in arthritic mice induced significantly less ova in oviducts and maturing follicles as compared to nonarthritic controls. Immunological factors yet to be elucidated may be involved in this ovarian dysfunction.

AB - Collagen-induced arthritis (CIA) in mice is a model of inflammatory polyarthritis that has many features similar to human rheumatoid arthritis. In rheumatoid arthritis, pregnancy leads to amelioration of the disease while exacerbation develops after delivery. We used the CIA model to elucidate the role of pregnancy on disease and vice versa. The onset of arthritis in pregnant mice was delayed in the B10.RIII strains immunized with native porcine type II collagen 7-12 days prior to syngeneic [B10.RIII (susceptible to CIA) x B10.RIII] and allogeneic (B10.RIII female x B10.K male that are CIA resistant) pregnancy. In contrast, when mice were immunized on days 1-6 of pregnancy, the onset of arthritis was earlier as compared wtih controls. In addition, once the mice developed CIA after delivery, the disease showed markedly rapid progression as compared to the control immunized group. Humoral immune responses to type II collagen showed significantly decreased levels on day 14 (at late stage of pregnancy) both in syngeneic and allogeneic postmating immunized pregnant mice. The same effect was also seen in allogeneic premating immunized pregnant mice on day 21 (at mid-stage of pregnancy). The levels of these antibodies increased after delivery. Subclasses of IgG1 and IgG(2a) antibodies to type II collagen were suppressed during pregnancy. In the pseudopregnant group, these antibodies showed deceased levels on day 14, but did not differ from the control groups on day 21 and 28. Some immunoregulatory changes may play a role in these alterations in pregnant arthritic mice. In comparison to the effects of syngeneic (susceptible x susceptible) pregnancy on CIA, allogeneic (susceptible female x resistant male) pregnancy seemed to be beneficial for the affected individuals. Litter size and mean birth weight were not affected by immunization of type II collagen. After onset of CIA, both syngeneic and allogeneic matings failed to produce offspring in arthritic female mice. The estrus cyclicity was highly disturbed in arthritic female mice and gonadotropin stimulation in arthritic mice induced significantly less ova in oviducts and maturing follicles as compared to nonarthritic controls. Immunological factors yet to be elucidated may be involved in this ovarian dysfunction.

UR - http://www.scopus.com/inward/record.url?scp=0022547440&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0022547440&partnerID=8YFLogxK

M3 - Article

C2 - 3740348

AN - SCOPUS:0022547440

VL - 11

SP - 44

EP - 54

JO - American Journal of Reproductive Immunology

JF - American Journal of Reproductive Immunology

SN - 1046-7408

IS - 2

ER -