straints on the primordial size distribution of
the asteroids. The newest models that started
the whole debate suggest that planetesimals
form through the clumping of small particles
(1, 2), predicting that asteroids that form
should initially be of large size. Morbidelli et
al. (6) modeled asteroid formation and found
that to reproduce the existing size-frequency
distribution of asteroids they must prefer-
entially form at sizes of about 100 km, add-
ing weight to the new theories. Morbidelli
et al., however, were unable to constrain the
size distribution below 100 km. A number
of later works modeled the primordial size-
frequency distribution of asteroids and found
wide-ranging results. Some matched that of
today’s asteroid belt (7, 8) and others found a
shallower distribution (9, 10). Delbo’ et al. (3)
provide the first estimate of the primordial
size-frequency distribution, confirming the
results of Klahr and Schreiber (10).
Although the work of Delbo’ et al. presents
a strong observational constraint, it is not
conclusive evidence. To link all remaining
background objects in other regions of the
main belt and for other compositions within
a family is no small task, and the authors
were able to take advantage of a specific set
of conditions in the inner part of the main
belt—namely, the smaller number of dark asteroids that exist in that region. This advantage no longer remains when one ventures
further out in the main belt. Additionally, although Delbo’ et al. constrain the primordial
size-frequency distribution of the darker asteroids, it remains to be shown if the brighter
ones that formed in a different location (11)
share the same formation characteristics.
Further work is required to understand if
more background bodies can be tied together
to families and if additional information can
be gleaned from this primordial family about
the earliest stages of solar system history. j
REFERENCES AND NOTES
1. A. Johansen etal.,Nature448, 1022 (2007).
2. J. N. Cuzzi, R. C. Hogan, K. Shariff, Astrophys.J. 687, 1432
3. M. Delbo’, K. Walsh, B. Bolin, C. Avdellidou, A. Morbidelli,
Science 357, 1026 (2017).
4. D. Nesvorný et al ., in Asteroids IV , P. Michel et al ., Eds.
(Univ. Arizona Press, 2015).
5. K. Hirayama, Astron.J. 31, 185 (1918).
6. A. Morbidelli, W. F. Bottke, D. Nesvorný, H. F. Levison,Icarus
204, 558 (2009).
7. A. Johansen, M. M. Lo w, P. Lacerda, M. Bizzarro, Sci.Adv. 1,
8. J.B.Simon, P.J.Armitage, R.Li,A.N.Youdin,Astrophys.J.
822, 55 (2016).
9. W. F. Bottke etal .,Icarus 175, 111 (2005).
10. H.Klahr, A.Schreiber, Inter. Astron. Union Symp. 318,1
11. T. S. Kruijer, C. Burkhardt, G. Budde, T. Kleine, Proc. Natl.
Acad. Sci. U.S.A. 114, 6712 (2017).
ACKNO WLEDGMEN TS
F. D. is supported by the National Aeronautics and Space
Administration under grant no. NNX12AL26G issued through
the Planetary Astronomy Program.
IMMUN OLOG Y
The balance between
immunity and inflammation
Lung immunity is calibrated to protect from inhaled
pathogens and avoid inflammation
By Darin L. Wiesner1,2 and
Bruce S. Klein1,2,3
Lungs execute two critical functions that can be at odds with one another: elimi- nating harmful toxins, particulates, and microbes; and exchanging gas through uninflamed structures—alveoli—to col- lect oxygen and discharge carbon dioxide. Lungs have a multilayered response to
unwanted invaders, offering physical barriers as well as arranging immune
cells at airway surfaces. Yet, lungs
have the “Goldilocks” challenge of
deploying this armory with just
the right amount of inflammation. Consequently, lung immunity must be choreographed so
that invaders are purged quickly,
inflammation tempered, and homeostasis preserved. In this issue,
two papers reveal how lung immunity handles these tasks and
what happens when things go
awry. Shlezinger et al. (1) on page
1037 unveil a clever trick that neutrophils play on inhaled fungal
spores to resist life-threatening
infections. This may reveal new
treatment strategies. On page 1014,
Sinclair et al. (2) report metabolic
derangements in dendritic cells
(DCs) that reprogram the allergic
response to inhaled particulates,
with implications for asthma.
In urban and rural air, 4 to 11%
of the fine particle mass contains
fungal spores (3). More than 300
million people suffer serious fun-gal-related diseases that kill more
than 1.6 million people annually
(4). More than 1 million fungal
species populate our planet, and
300 are human pathogens (5). Aspergillus is
a common cause of systemic infection in people with impaired immunity owing to AIDS,
complications associated with chemotherapy,
or treatments for inflammatory disorders, often with high fatality rates.
Shlezinger et al. studied the spores (
conidia) from Aspergillus fumigatus. Every
day, humans each inhale 103 to 1010 of these
seemingly innocuous airborne conidia. In
addition to being a common aeroallergen,
1Department of Pediatrics, School of Medicine
and Public Health, University of Wisconsin-Madison, Madison, WI 53792, USA. 2Department
of Internal Medicine, School of Medicine and
Public Health, University of Wisconsin-Madison,
Madison, WI 53792, USA. 3Department of
Medical Microbiology and Immunology, School
of Medicine and Public Health, University of
Wisconsin-Madison, Madison, WI 53792, USA.
New mechanisms revealed in lung immunity
Neutrophils fght Aspergillus infection, which can be counteracted
by Af Bir1 expression. The regulation of granulocyte responses
to aeroallergens through DC metabolism could infuence the
occurrence of asthma.
Asthma Cell death in
Bir1 is induced in A. fumigatus
conidia to prevent PCD that is
induced by neutrophils. This could
lead to invasive aspergillosis.
PCD of spore
8 SEP TEMBER 2017 • VOL 357 ISSUE 6355 973
The balance of
Lung immunity faces the
of responding with
just the right amount