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Y. Bai et al.
recent discovery has indicated that aspirin, a very widely used anti-inflammatory
drug, triggers the production of novel anti-inflammatory resolvins and lipoxins after
binding to its target, COX-2, which may be an explanation for its well-known painkilling action [8].
Besides PUFAs, platelet-activating factor (PAF) is another multifunctional
endogenous compound. There are two pathways for PAF biosynthesis, the remodeling and the de novo pathway. The remodeling pathway, in which PAF is synthesized by substitution of an arachidonoyl moiety with an acetyl in 1-O-alkyl-2arachidonoylglycerophosphocholine, is believed to be the primary source of PAF,
especially during inflammation. The de novo pathway, in which 1-O-alkyl-snglycero-3-phosphate is acetylated, hydrolyzed to 1-O-alkyl-2-acetyl-sn-glycerol, and
converted to PAF by a dithiothreitol-insensitive CDP-cholinephospho-transferase,
has been proposed as a source of PAF for housekeeping physiological roles. Besides
the activation of platelets, as its name indicates, PAF initiates inflammation by action
on the PAF receptor [9]. Additionally, it has been shown that PAF receptor activation
is neuroprotective and that PAF induces neuronal apoptosis independent of the PAF
receptor [10]. The platelet-activating factor is also believed to play a non-pathological
role in stimulating uterine contraction at the end of pregnancy.
3 Host–Microbe Co-metabolism
3.1 Presence and Function of the Human Microbiota
As the human commensal microorganisms (i.e., the microbiota) are estimated to be
more than ten times greater compared to those of human somatic and germ cells,
they are believed to explain the individual differences of normal physiology and
predisposition to disease. Therefore, a project named the human microbiome project
(HMP) was launched after the human genome project [1]. The human microbiome
project led to the discovery that the diversity and abundance of each habitat’s signature microbes vary largely, but the microbiota of the specific niche of an individual
is quite stable [11]. A further data study named the expanded HMP has revealed
a more complicated atlas of personalized microbiome composition, function, and
dynamics [12]. According to the HMP, a “long tail” of low-abundance genes and
pathways probably encodes many uncharacterized bioactivities and metabolites in
the microbiomes. Therefore, host–microbe co-metabolism is believed to be essential
in elucidating the roles of the microbiota in health and diseases [11].
The co-metabolism of the chemicals of host and its microbiota can be categorized roughly into three patterns: the first pattern involves the chemicals produced
solely by microbes, like the production of vitamins, siderophores, and short-chain
fatty acids [13]. The second pattern involves those chemicals produced solely by the
host, like the production of primary bile acids [14] and most compounds included
in Sect. 2. The third pattern involves the chemicals produced collaboratively by the
Y. Bai et al.
recent discovery has indicated that aspirin, a very widely used anti-inflammatory
drug, triggers the production of novel anti-inflammatory resolvins and lipoxins after
binding to its target, COX-2, which may be an explanation for its well-known painkilling action [8].
Besides PUFAs, platelet-activating factor (PAF) is another multifunctional
endogenous compound. There are two pathways for PAF biosynthesis, the remodeling and the de novo pathway. The remodeling pathway, in which PAF is synthesized by substitution of an arachidonoyl moiety with an acetyl in 1-O-alkyl-2arachidonoylglycerophosphocholine, is believed to be the primary source of PAF,
especially during inflammation. The de novo pathway, in which 1-O-alkyl-snglycero-3-phosphate is acetylated, hydrolyzed to 1-O-alkyl-2-acetyl-sn-glycerol, and
converted to PAF by a dithiothreitol-insensitive CDP-cholinephospho-transferase,
has been proposed as a source of PAF for housekeeping physiological roles. Besides
the activation of platelets, as its name indicates, PAF initiates inflammation by action
on the PAF receptor [9]. Additionally, it has been shown that PAF receptor activation
is neuroprotective and that PAF induces neuronal apoptosis independent of the PAF
receptor [10]. The platelet-activating factor is also believed to play a non-pathological
role in stimulating uterine contraction at the end of pregnancy.
3 Host–Microbe Co-metabolism
3.1 Presence and Function of the Human Microbiota
As the human commensal microorganisms (i.e., the microbiota) are estimated to be
more than ten times greater compared to those of human somatic and germ cells,
they are believed to explain the individual differences of normal physiology and
predisposition to disease. Therefore, a project named the human microbiome project
(HMP) was launched after the human genome project [1]. The human microbiome
project led to the discovery that the diversity and abundance of each habitat’s signature microbes vary largely, but the microbiota of the specific niche of an individual
is quite stable [11]. A further data study named the expanded HMP has revealed
a more complicated atlas of personalized microbiome composition, function, and
dynamics [12]. According to the HMP, a “long tail” of low-abundance genes and
pathways probably encodes many uncharacterized bioactivities and metabolites in
the microbiomes. Therefore, host–microbe co-metabolism is believed to be essential
in elucidating the roles of the microbiota in health and diseases [11].
The co-metabolism of the chemicals of host and its microbiota can be categorized roughly into three patterns: the first pattern involves the chemicals produced
solely by microbes, like the production of vitamins, siderophores, and short-chain
fatty acids [13]. The second pattern involves those chemicals produced solely by the
host, like the production of primary bile acids [14] and most compounds included
in Sect. 2. The third pattern involves the chemicals produced collaboratively by the