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. Author manuscript; available in PMC: 2011 Jan 25.
Published in final edited form as: Mol Oral Microbiol. 2010 Jan 25;25(1):25–37. doi: 10.1111/j.2041-1014.2009.00562.x

Table 1.

Effects of aging on phagocytic cell function*

Functional status Phagocytes
Neutrophils Macrophages
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Reduced Receptor recruitment to lipid rafts
Signal transduction (e.g., Ca2+ influx, phosphorylation of ERK, p38, Akt, PLC-γ)
Chemotaxis
Phagocytosis		 Signal transduction (e.g., total levels and/or activation of STAT-1α, p38 & JNK MAPKs, MyD88, NF-κB)
Chemotaxis
Cytokine production (IL-6, TNF-α, MIP-1α, MIP-1β, MIP-2)
Reactive oxygen species production
Maintained Total cell number
Receptor expression (GM-CSFR, TLR2, TLR4, CD14, CD11b)
Apoptosis (spontaneous)		 Expression of IFN-γR and TLRs (TLR2, TLR4, TLR5, TLR6)
Phagocytic receptor expression (CD14, CD11b, CD18, CD36, mannose receptor [CD206], dectin-1, scavenger receptor-AI)
Phagocytosis (?)
Expression of TLR negative regulators (e.g., SOCS-1, IRAK-M, A20, PPAR-γ)
Increased Apoptosis (under priming conditions) Receptors involved in inflammation amplification (C5aR, TREM-1)
PGE2 production
Controversial or both increase/decrease observed Reactive oxygen species production Nitric oxide production and intracellular killing
TLR1 (decreased in human monocytes; unaltered in mouse macrophages)
*

This compilation is based on a great number of studies, mainly using mouse or human cells, and original work has been cited in excellent specialized reviews (Butcher et al., 2000; Fulop et al., 2004; Gomez et al., 2008; Kovacs et al., 2009; Plowden et al., 2004; Solana et al., 2006; Stout and Suttles 2005).