The acute phase response of rats to soman intoxication

The Immune System as a Target for Chemical Warfare Agents

“…In addition, a decreased number of cells in the spleen and thymus (Ladics et al, 1994), an inhibition of chemotaxis in neutrophils (Ward, 1968), inhibition of monocyte accessory functions, and inhibition of interleukin-2 production (Pruett and Chambers, 1988;Casale et al, 1993) were reported following the exposure to OPs, at relatively high toxic doses. Similar activation of some immune functions involving "acute phase response," such as increase in the synthesis of acute phase proteins, increase in release of histamine from basophile leukocytes, and activation of macrophages, was observed following exposure to soman (Newball et al, 1986;Sevaljevic et al, 1992). They demonstrated that lymphocyte proliferation to phytohemaglutinin in vitro was decreased in the presence of OPs.…”

The Immune System as a Target for Chemical Warfare Agents

“…In addition, a decreased number of cells in the spleen and thymus (Ladics et al, 1994), an inhibition of chemotaxis in neutrophils (Ward, 1968), inhibition of monocyte accessory functions, and inhibition of interleukin-2 production (Pruett and Chambers, 1988;Casale et al, 1993) were reported following the exposure to OPs, at relatively high toxic doses. Similar activation of some immune functions involving "acute phase response," such as increase in the synthesis of acute phase proteins, increase in release of histamine from basophile leukocytes, and activation of macrophages, was observed following exposure to soman (Newball et al, 1986;Sevaljevic et al, 1992). They demonstrated that lymphocyte proliferation to phytohemaglutinin in vitro was decreased in the presence of OPs.…”

The organophosphate‐induced acute‐phase response is characterized by synthesis of α1‐acid glycoprotein that exhibits an immunomodulatory effect

“…Inhibition of the Con A-stimulated proliferation of normal thymocytes in the presence of sera taken after paraoxon administration was ascribed to increased corticosterone concentrations. Soman also produces a considerable immunosuppressive effect in rats (Clement, 1985;Tevaljevic et al, 1992). However, Clement showed that in adrenalectomized mice, soman exerted an immunosuppressive response as well, suggesting the involvement of adrenal-independent mechanisms.…”

“…This implies that the molecular mechanisms that operated after paraoxon and soman poisoning were similar to those observed during the turpentine-induced AP response. However, the combinations of mediators that regulate these processes appear to be injury-specific (Birch and Schreiber, 1986;Baumann, 1989;Tevaljevic et al, 1992;Poznanovic et al, 1997).…”

The Influence of Single or Repeated Low‐Level Sarin Exposure on Immune Functions of Inbred BALB/c Mice

“…Recent results demonstrate that organophosphate‐induced modulation of immune functions can involve not only their suppression but also their activation (Johnson et al 2002). The activation of some immune functions involved in “acute phase response” such as an increase in the synthesis of acute phase proteins, increase in release of histamine from basophile leukocytes and activation of macrophages, was observed following exposure to soman (Newball et al 1986; Sevaljevic et al 1987, 1989 & 1992).…”

“…The modulation of immune functions following low‐level organophosphate exposure seems to be very complex. Some immune functions are probably stimulated due to the development of “acute phase response” generally characterized for inflammatory reactions of organophosphate‐exposed organisms (Sevaljevic et al 1987, 1989 & 1992). Other immune functions are suppressed due to immunotoxicity of organophosphorous compounds.…”

The Immune System as a Target for Chemical Warfare Agents

“…In addition, a decreased number of cells in the spleen and thymus (Ladics et al, 1994), an inhibition of chemotaxis in neutrophils (Ward, 1968), inhibition of monocyte accessory functions, and inhibition of interleukin-2 production (Pruett and Chambers, 1988;Casale et al, 1993) were reported following the exposure to OPs, at relatively high toxic doses. Similar activation of some immune functions involving "acute phase response," such as increase in the synthesis of acute phase proteins, increase in release of histamine from basophile leukocytes, and activation of macrophages, was observed following exposure to soman (Newball et al, 1986;Sevaljevic et al, 1992). They demonstrated that lymphocyte proliferation to phytohemaglutinin in vitro was decreased in the presence of OPs.…”

The organophosphate‐induced acute‐phase response is characterized by synthesis of α1‐acid glycoprotein that exhibits an immunomodulatory effect

“…Inhibition of the Con A-stimulated proliferation of normal thymocytes in the presence of sera taken after paraoxon administration was ascribed to increased corticosterone concentrations. Soman also produces a considerable immunosuppressive effect in rats (Clement, 1985;Tevaljevic et al, 1992). However, Clement showed that in adrenalectomized mice, soman exerted an immunosuppressive response as well, suggesting the involvement of adrenal-independent mechanisms.…”

“…This implies that the molecular mechanisms that operated after paraoxon and soman poisoning were similar to those observed during the turpentine-induced AP response. However, the combinations of mediators that regulate these processes appear to be injury-specific (Birch and Schreiber, 1986;Baumann, 1989;Tevaljevic et al, 1992;Poznanovic et al, 1997).…”

The Influence of Single or Repeated Low‐Level Sarin Exposure on Immune Functions of Inbred BALB/c Mice

“…Recent results demonstrate that organophosphate‐induced modulation of immune functions can involve not only their suppression but also their activation (Johnson et al 2002). The activation of some immune functions involved in “acute phase response” such as an increase in the synthesis of acute phase proteins, increase in release of histamine from basophile leukocytes and activation of macrophages, was observed following exposure to soman (Newball et al 1986; Sevaljevic et al 1987, 1989 & 1992).…”

“…The modulation of immune functions following low‐level organophosphate exposure seems to be very complex. Some immune functions are probably stimulated due to the development of “acute phase response” generally characterized for inflammatory reactions of organophosphate‐exposed organisms (Sevaljevic et al 1987, 1989 & 1992). Other immune functions are suppressed due to immunotoxicity of organophosphorous compounds.…”

The Immune System as a Target for Chemical Warfare Agents

“…In addition, a decreased number of cells in the spleen and thymus (Ladics et al, 1994), an inhibition of chemotaxis in neutrophils (Ward, 1968), inhibition of monocyte accessory functions, and inhibition of interleukin-2 production (Pruett and Chambers, 1988;Casale et al, 1993) were reported following the exposure to OPs, at relatively high toxic doses. Similar activation of some immune functions involving "acute phase response," such as increase in the synthesis of acute phase proteins, increase in release of histamine from basophile leukocytes, and activation of macrophages, was observed following exposure to soman (Newball et al, 1986;Sevaljevic et al, 1992). They demonstrated that lymphocyte proliferation to phytohemaglutinin in vitro was decreased in the presence of OPs.…”

The organophosphate‐induced acute‐phase response is characterized by synthesis of α1‐acid glycoprotein that exhibits an immunomodulatory effect

“…Inhibition of the Con A-stimulated proliferation of normal thymocytes in the presence of sera taken after paraoxon administration was ascribed to increased corticosterone concentrations. Soman also produces a considerable immunosuppressive effect in rats (Clement, 1985;Tevaljevic et al, 1992). However, Clement showed that in adrenalectomized mice, soman exerted an immunosuppressive response as well, suggesting the involvement of adrenal-independent mechanisms.…”

“…This implies that the molecular mechanisms that operated after paraoxon and soman poisoning were similar to those observed during the turpentine-induced AP response. However, the combinations of mediators that regulate these processes appear to be injury-specific (Birch and Schreiber, 1986;Baumann, 1989;Tevaljevic et al, 1992;Poznanovic et al, 1997).…”

The Influence of Single or Repeated Low‐Level Sarin Exposure on Immune Functions of Inbred BALB/c Mice

“…Recent results demonstrate that organophosphate‐induced modulation of immune functions can involve not only their suppression but also their activation (Johnson et al 2002). The activation of some immune functions involved in “acute phase response” such as an increase in the synthesis of acute phase proteins, increase in release of histamine from basophile leukocytes and activation of macrophages, was observed following exposure to soman (Newball et al 1986; Sevaljevic et al 1987, 1989 & 1992).…”

“…The modulation of immune functions following low‐level organophosphate exposure seems to be very complex. Some immune functions are probably stimulated due to the development of “acute phase response” generally characterized for inflammatory reactions of organophosphate‐exposed organisms (Sevaljevic et al 1987, 1989 & 1992). Other immune functions are suppressed due to immunotoxicity of organophosphorous compounds.…”