[[Image:Bacterial innate response.jpg|thumb|right|150px|Bacterial responses - B. Catchpole, RVC 2008]]
[[Image:Bacterial innate response.jpg|thumb|right|150px|Bacterial responses - B. Catchpole, RVC 2008]]
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The innate response to bacterial infection lies in its first-response role of detection of a foreign organism. By using the above described tools of [[Recognition of Microorganisms|Pattern-Recognition Receptors (PRRs)]], the innate response flags up problems while the [[:Category:Adaptive Immune System|adaptive]] response gets itself organized. Once a foreign organism is detected, the innate system responds by engaging in cell warfare via [[Phagocytosis|phagocytosis]] and triggering the [[:Category:Inflammation|inflammatory]] response. The release of inflammatory [[Cytokines|cytokines]] will cause an increase in vasodilation, vascular permeability and an influx of white blood cells. [[Neutrophils|Neutrophils]] take on their primary role as phagocytes in this phase. In addition, systemic effects of inflammatory cytokines will sustain a rise in core temperature (fever), the release of acute phase proteins from the [[Liver - Anatomy & Physiology|liver]], and bone marrow mobilization as the need for white blood cells production is increased. Acute phase proteins will bind to bacterial cell walls, enhancing neutrophil, macrophage, and [[Complement|complement]]-initiated phagocytosis.
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The innate response to bacterial infection lies in its first-response role of detection of a foreign organism. By using the tools of [[Recognition of Microorganisms|Pattern-Recognition Receptors (PRRs)]], the [[:Category:Innate Immune System|innate]] response flags up problems while the [[:Category:Adaptive Immune System|adaptive]] response gets itself organized.
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Once a foreign organism is detected, the innate system responds by engaging in cell warfare via [[Phagocytosis|phagocytosis]] and triggering the [[:Category:Inflammation|inflammatory]] response. The release of inflammatory [[Cytokines|cytokines]] will cause an increase in vasodilation, vascular permeability and an influx of white blood cells. [[Neutrophils|Neutrophils]] take on their primary role as phagocytes in this phase. In addition, systemic effects of inflammatory cytokines will sustain a rise in core temperature (fever), the release of acute phase proteins from the [[Liver - Anatomy & Physiology|liver]], and [[Bone Marrow|bone marrow]] mobilization as the need for white blood cells production is increased. Acute phase proteins will bind to bacterial cell walls, enhancing neutrophil, [[Macrophages|macrophage]], and [[Complement|complement]]-initiated phagocytosis.
<big>'''Also see [[Immunity to Bacteria]]'''</big>
<big>'''Also see [[Immunity to Bacteria]]'''</big>