Ammonia, dust, microorganisms, and lipopolysaccharide (LPS) are ubiquitous in chicken houses. Lipopolysaccharide is a cell wall component of Gram-negative bacteria that activates pulmonary and immune activities that negatively affect health and performance of commercial broilers. Using intravenous (i.v.) administration of LPS as a model to examine the effects of LPS on pulmonary hemodynamics, a transient increase in pulmonary arterial pressure (PAP), or a pulmonary hypertensive (PH) response, was observed during the first hour post-LPS administration. The observed LPS-induced PH response was shown to be modulated by vasoactive mediators such as nitric oxide (NO), a vasodilator produced by endothelial cells and monocytes and macrophages, and serotonin (5-HT), a vasoconstrictor released by thrombocytes. It was also observed that a second i.v. LPS administration did not induce another PH response, unless 4- to 5-d had passed between the first and second LPS injection—suggesting non-responsiveness, or tolerance, of the immune response or pulmonary vasculature for several days post-LPS administration. The objective of this dissertation was to examine the effect of i.v. LPS administration in chickens on innate immune response activities in vivo and in vitro. Specifically, a time course approach (hours and days-post i.v. LPS) was used to examine the effects of i.v. LPS administration in chickens on (1) plasma NO levels (Chapter 2); (2) leukocyte proportions and concentrations in whole blood, and in peripheral blood mononuclear cell (PMNC) proportions in PMNC cultures prepared from blood, as well as, in vitro NO production by monocytes in PMNC cultures with and without further in vitro LPS stimulation (Chapter 3); and (3) key aspects of innate/adaptive immune activity in response to a second i.v. LPS administration given at 24 h intervals over a seven day period after the first LPS injection (Chapter 4). Plasma NO levels of chickens increased by 3 h, peaked at 5- to 6-h, and returned to normal by 10 h after an i.v. LPS injection, reflecting activation of inducible NO synthase in vivo. Leukocyte concentrations, specifically monocytes, were altered after an i.v. LPS injection, including a substantial drop in concentrations by 1 h post-LPS injection. Although fewer in numbers, the monocytes present in the blood samples produced NO in culture in response to in vitro LPS stimulation at levels similar to those of monocytes from non-LPS-injected chickens. The drop in monocytes in blood samples obtained 1 h post-LPS injection appeared to be due to leukocyte attachment to the endothelium after an LPS injection preventing monocytes from entering the needle during blood collection. Using key indices of the effects of i.v. LPS administration identified in Chapter 2 and 3 (e.g., elevated plasma NO levels at 6 h and reduced leukocyte levels at 1 h post-i.v. LPS injection) as end-point measurements of i.v. LPS responsiveness, it was found that chickens were responsive to a second i.v. LPS administration given at 24 hour intervals for 7 days after the first LPS administration. Hence, unlike the PH response which was tolerant to a second i.v. LPS administration up to 5 days after the first injection, there were no indications of tolerance regarding the LPS initiated innate immune activities examined here. Additionally, analysis of LPS-specific antibody levels revealed elevated levels at 4- to 6-d post i.v. LPS injection, at a time when pulmonary responsiveness returned to normal, suggesting that LPS-neutralization by antibodies is not responsible for the observed PH LPS tolerance.