T Cell Proliferative Response Following Sepsis in Neonatal Rats

Dallal, Ousama; Ravindranath, Thyyar; Choudhry, M. A.; Kohn, A.; Muraskas, Jonathan; Sayeed, M. M.

doi:10.1097/00024382-199906001-00279

Cited by 1 publication

(5 citation statements)

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“…This is consistent with our preliminary studies which showed that Tcell proliferation is less suppressed in septic pups pretreated with COX-2 inhibitor than in untreated septic pups or those pretreated with COX-1 inhibitor [11]. It is interesting to note that pretreatment of pups with COX-2 inhibitor totally prevented the sepsis-induced suppression of T-cell [Ca 2+ ] i response while, in the previous study, this treatment only partially improved T-cell proliferation [11]. This could be due to the possible suppression of Tcell proliferation via mechanisms that may not be totally dependent on prostaglandins.…”

Section: Discussionsupporting

confidence: 93%

“…The results of this study and the results of our previous study on T-cell proliferative response in septic neonatal rats [11] are consistent with the studies in adult rats. However, whereas the attenuation in T-cell [Ca 2+ ] i mobilization in adult rats occurred within the first day following sepsis induction, and was followed by the suppression of the proliferative response on day 2, the suppression in both T-cell [Ca 2+ ] i mobilization and proliferation in neonatal pups occurred within 24 h after sepsis.…”

Section: Discussionsupporting

confidence: 92%

“…The prevention of T-cell suppression with COX-2 inhibitor implies that the induced and not necessarily the constitutively formed prostaglandins are responsible for the sepsis-induced attenuation of the [Ca 2+ ] i signaling in splenic T cells from septic neonatal rats. This is consistent with our preliminary studies which showed that Tcell proliferation is less suppressed in septic pups pretreated with COX-2 inhibitor than in untreated septic pups or those pretreated with COX-1 inhibitor [11]. It is interesting to note that pretreatment of pups with COX-2 inhibitor totally prevented the sepsis-induced suppression of T-cell [Ca 2+ ] i response while, in the previous study, this treatment only partially improved T-cell proliferation [11].…”

Section: Discussionsupporting

confidence: 91%

“…Previous studies from our laboratory have demonstrated that alteration in T-cell [Ca 2+ ] i mobilization precedes the suppression of T-cell proliferative response in septic adult rats [14], suggesting a temporal relationship between the two events during sepsis. Our preliminary studies have shown a sepsis-induced suppression of T-cell proliferative response in septic neonatal rats as well [11]. Based on these results we can conclude that, in neonatal rats, attenuation in [Ca 2+ ] i mobilization likely contributes to the T-cell proliferative response suppression which occurs during sepsis.…”

Section: Discussionsupporting

confidence: 57%

“…Such suppression can alter the host defense against sepsis [9,10]. T-cell proliferation suppression has also been demonstrated in septic rat pups in preliminary studies performed in our laboratory [11].…”

Section: Introductionmentioning

confidence: 94%

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Sepsis-Induced Alteration in T-Cell Ca<sup>2+</sup> Signaling in Neonatal Rats

et al. 2001

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Sepsis-induced suppression in T-cell proliferation follows deranged Ca²⁺ signaling in adult rats. In preliminary studies, we observed suppression in T-cell proliferation in septic neonatal rats as well. In this study, we assessed splenic T-cell cytosolic Ca²⁺ concentration, [Ca²⁺]_i, as its elevation plays an important role in T-cell proliferation. Also, we investigated the role of PGE₂ in sepsis-related changes in T-cell [Ca²⁺]_i in animals pretreated with cyclooxygenase-1 (COX-1) inhibitor (resveratrol) and cyclooxygenase-2 (COX-2) inhibitor (NS-398). Sepsis was induced in 15-day-old rat pups by intraperitoneal implantation of fecal pellets containing Escherichia coli and Bacteroides fragilis. The sham group consisted of pups implanted with sterile fecal pellets. Septic and sham pups were sacrificed 24 h after implantation and their spleens were removed. The spleens from sham and septic pups, along with spleens from unoperated control pups, were processed for single cell suspensions, and T cells were isolated using nylon wool columns. Fura-2 fluorophotometry was employed for the measurement of [Ca²⁺]_i (in nM units) in T cells stimulated with concanavalin A (ConA). Our results show that ConA-mediated T-cell [Ca²⁺]_i response is significantly suppressed in septic neonatal rats. Pretreatment of pups with COX-2, but not COX-1 inhibitor, prevented the decrease in the [Ca²⁺]_i response. These findings suggest that PGE₂ might induce the attenuation in T-cell Ca²⁺ signaling during sepsis in neonatal rats.