@booklet {1673,
	title = {Inflammation: more than one explanation},
	journal = {Environmental Health Perspectives},
	volume = {103},
	number = {11},
	year = {1995},
	pages = {985},
	abstract = {I read with interest the EHP supplement
on oxygen radicals and lung injury (vol.
102, supplement 10). I would like to
take this opportunity to comment about
this supplement and raise a key issue
concerning the major concepts regarding
the mechanisms of cellular injury in
inflammatory diseases.
As an active investigator in this field
of research, I cannot fully understand
why there was no mention in the supplement
about the basic understanding that
cellular damage in inflammation is multifactorial.
The nonexpert reader of this
supplement might receive an erroneous
impression that oxygen radicals, per se,
are the exclusive toxic agonists that
induce cellular injury. Many in this field
share the view that cellular damage in
inflammatory diseases might be caused
by a "coordinated cross-talk" among oxidants,
membrane-damaging agents, proteinases,
arachidonic acid metabolites,
phospholipases, cationic proteins, and
cytokines. All these agents are likely to be
present in sites of infection and inflammation.
But sadly, none of the publications
elaborating on this multifactorial
view are quoted in modern textbooks or
in symposia on inflammation and
inflammatory diseases. Instead, the literature
is filled with publications that insist
on a single agonist, be it an oxidant, a
protease, a cytokine, etc., in experimental
models. No attempt to integrate the various
agonists into the full picture is made.
Several of our publications (1-7) deal
with synergistic interactions among multiple
proinflammatory agonists in cellular
injury during inflammation. I believe
that this issue is important, timely, and
might contribute to an understanding of
how drugs, chemicals, and xenobiotics
function in vivo.
Isaac Ginsburg
Hadassah School of Dental Medicine
Hebrew University
Jerusalem},
	author = {Isaac Ginsburg}
}
