Thus it is evident from a number of various facts, that the eosinophil
cells found in the tissues are not formed there, but have immigrated
from the blood-stream. It naturally often happens that this appearance
is not preserved equally distinctly in all cases. For, as has been seen
in the ordinary polynuclear leucocytes, the immigrated polynuclear
eosinophils may similarly change to mononuclear cells; they may perhaps
settle down, and approximate to the character of fixed connective tissue
cells. Such appearances may readily give rise to the view that in this
case the reverse nuclear metamorphosis has occurred; that is a
progressive development from mononuclear eosinophil to polynuclear
cells.
In agreement with Goldmann, Jadassohn and H. F. Mueller, we believe that
the only admissible explanation for the facts mentioned above is that
the eosinophil cells obey specific chemiotactic stimuli. By this
hypothesis we can easily understand eosinophil leucocytosis, the
presence of eosinophil cells in exudations and secretions, and the local
accumulation of this kind of cell.
As to the nature of these chemiotactically active substances, we can so
far only surmise. From amongst the clinical phenomena capable of
throwing light on this subject we mention once more the fact, that the
metabolic products of bacteria repel the eosinophil cells.
The opposed behaviour of eosinophil and neutrophil cells is
very well illustrated by a case of Leichtenstern:
"In a very anaemic almost moribund patient with Ankylostomias
there were found 72% eosinophil cells in the blood in 1897. The
patient contracted a croupous pneumonia, and in the high
febrile period of the disease the number of eosinophils sank to
6-7%, and rose again after the termination of the pneumonia to
54%. After removal of the worm the number at once fell to 11%.
In the year 1898 the patient harboured but a very few
Ankylostomata; Charcot's crystals were no longer present in the
faeces; the number of the eosinophils amounted to 8%."
Public-domain text, read in full here on John Shaqi.
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